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1.
Bol. latinoam. Caribe plantas med. aromát ; 24(1): 47-61, ene. 2025. ilus, graf
Article in English | LILACS | ID: biblio-1584582

ABSTRACT

This study investigates the efficacy and mechanisms of Kuanxiong Aerosol (KXA) on coronary microvascular dysfunction (CMD) in rats. Thirty-two Sprague-Dawley rats were divided into control, model, KXA, and nicorandil groups, receiving respective treatments for three weeks. The CMD model was established byinjecting lauric acid into the left ventricle. Compared to the model group, the KXA group showed significant reductions in serum CK-MB, LDH, cTnI, ET-1, TNF-α, IL-6, MDA, and ROS (p<0.01) and increased NO and SOD levels (p<0.01). KXA mitigated apoptosis and ameliorated CMD-associated pathological alterations. Pretreatment with KXA improves endothelial function and microvascular structure by counteracting inflammation, oxidative stress, and apoptosis, thereby improving CMD.


Este estudio investiga la eficacia y los mecanismos del Aerosol de Kuanxiong (KXA) sobre la disfunción microvascular coronaria (CMD) en ratas. Treinta y dos ratas Sprague-Dawley se dividieron en grupos de control, modelo, KXA y nicorandil, recibiendo los respectivos tratamientos durante tres semanas. El modelo de CMD se estableció inyectando ácido láurico en el ventrículo izquierdo. En comparación con el grupo modelo, el grupo KXA mostró reducciones significativas en los niveles séricos de CK-MB, LDH, cTnI, ET-1, TNF-α, IL-6, MDA y ROS (p<0.01) y un aumento en los niveles de NO y SOD (p<0.01). KXA mitigó la apoptosis y mejoró las alteraciones patológicas asociadas con la CMD. El pretratamiento con KXA mejora la función endotelial y la estructura microvascular al contrarrestar la inflamación, el estrés oxidativo y la apoptosis, mejorando así la CMD.


Subject(s)
Animals , Rats , Coronary Artery Disease/drug therapy , Aerosols , Rats, Sprague-Dawley , Apoptosis , Oxidative Stress , Coronary Circulation/drug effects , Anti-Inflammatory Agents/pharmacology
2.
Int. j. morphol ; 42(4): 905-910, ago. 2024. ilus, tab
Article in English | LILACS | ID: biblio-1569245

ABSTRACT

SUMMARY: Underage drinking has become a major public concern having a negative impact on the growth and development of the skeleton. Peak bone mass is attained during adolescence hence the aim of the study was to investigate the effect of acute binge alcohol consumption on trabecular morphometry and tensile strength of the adolescent mandible in the Sprague Dawley (SD) rat. The study comprised of 24 SD rats, aged 7 weeks, placed into either the alcohol-exposed [n=12 (6 males and 6 female)] or pair-fed control group [n=12 (6 male and 6 female)]. The treatment of the groups was as follows; the alcohol exposed group and the pair-fed control were administered a single daily dose of 3 g/kg of 20 % alcohol 3 days a week (alternate days) for 7 days and a caloric equivalent dose of maltose dextrin via oral gavage, respectively. The animals were terminated on day 7 via pentobarbital injection. The mandibles were harvested and scanned using a Nikon XTH 255L 3D-microCT scanner (Nikon Metrology, Leuven, Belgium), and biomechanical tests were done using a Shimadzu universal tensile strength testing machine (China). Following scanning and reconstruction, the trabecular morphometry was assessed using Volume Graphics Studio® software. A 3-point bending test was used to evaluate the tensile strength of the bone. Findings from our study showed changes in some trabecular parameters in the female alcohol-exposed group, while the male groups remained unaffected. No changes in tensile strength were seen when comparing male pair-fed control and alcohol-exposed groups and when comparing female pair-fed control and alcohol-exposed groups. Trabecular and tensile strength differences were observed between the sexes when comparing male pair-fed control and alcohol-exposed groups to female pair-fed control and alcohol-exposed groups. These findings do suggest that acute binge alcohol consumption has detrimental effects on the bone micro-architecture in female alcohol-exposed rats and that differences are seen between the sexes.


El consumo de alcohol entre menores de edad se ha convertido en una importante preocupación pública que tiene un impacto negativo en el crecimiento y desarrollo del esqueleto. La masa ósea máxima se alcanza durante la adolescencia, por lo que el objetivo del estudio fue investigar el efecto del consumo excesivo de alcohol en forma aguda sobre la morfometría trabecular y la resistencia a la tracción de la mandíbula en ratas adolescente Sprague Dawley (SD). El estudio estuvo compuesto por 24 ratas, de 7 semanas de edad, colocadas en el grupo control expuesto al alcohol [n=12 (6 machos y 6 hembras)] y alimentado en parejas [n=12 (6 machos y 6 hembras)]. El tratamiento de los grupos fue el siguiente; al grupo expuesto al alcohol y al control alimentado en parejas se les administró una dosis única diaria de 3 g/kg de alcohol al 20 % 3 días a la semana (días alternos) durante 7 días y una dosis equivalente calórica de maltosa dextrina mediante sonda oral, respectivamente. Los animales fueron sacrificados el día 7 mediante inyección de pentobarbital. Las mandíbulas se recolectaron y se escanearon utilizando un escáner 3D-microCT Nikon XTH 255L (Nikon Metrology, Lovaina, Bélgica), y las pruebas biomecánicas se realizaron utilizando una máquina de prueba de resistencia a la tracción universal Shimadzu (China). Después del escaneo y la reconstrucción, la morfometría trabecular se evaluó utilizando el software Volume Graphics Studio®. Se utilizó una prueba de flexión de 3 puntos para evaluar la resistencia a la tracción del hueso. Los hallazgos de nuestro estudio mostraron cambios en algunos parámetros trabeculares en el grupo de hembras expuestas al alcohol, mientras que los grupos de machos no se vieron afectados. No se observaron cambios en la resistencia a la tracción al comparar los grupos control de machos alimentados en parejas y los grupos expuestos al alcohol y al comparar los grupos control de las hembras alimentadas en parejas y los grupos expuestos al alcohol. Se observaron diferencias trabeculares y de resistencia a la tracción entre los sexos al comparar los grupos control de los machos alimentados en parejas y expuestos al alcohol con los grupos de control de hembras alimentadas en parejas y expuestas al alcohol. Estos hallazgos sugieren que el consumo excesivo de alcohol tiene efectos perjudiciales sobre la microarquitectura ósea en ratas hembras expuestas al alcohol y que se observan diferencias entre los sexos.


Subject(s)
Animals , Male , Female , Rats , Ethanol/toxicity , Binge Drinking , Mandible/drug effects , Tensile Strength , Biomechanical Phenomena , Bone Density , Sex Factors , Rats, Sprague-Dawley , Disease Models, Animal , Blood Alcohol Content , Cancellous Bone/drug effects
3.
Int. j. morphol ; 42(4): 1102-1110, ago. 2024. ilus, tab
Article in English | LILACS | ID: biblio-1569244

ABSTRACT

SUMMARY: Aging is an inevitable biological process that affects the function of all organs, including the adrenal gland, which is essential for producing steroid hormones that regulate metabolism, stress response, and immune activation. Understanding how aging affects the morphology of this gland is crucial to developing interventions to mitigate its adverse effects. Thus, this study aimed to describe the morphoquantitative alterations of the adrenal gland in senescent Sprague Dawley rats compared to adult rats. Twelve male rats were divided into 6 adult rats aged 6 months (group A) and 6 senescent rats aged 36 months (group S). Histopathological studies, quantification of collagen fibers types I and III, and stereological analysis were performed to determine the volume density (Vv), surface area (Sv), and number (Nv) of the nuclei of the zona fasciculata cells. Adrenal gland tissue from group S presented dysplasia, metaplasia, intracellular fat accumulation, fibrosis, blood vessel dilation, and increased presence of apoptotic cells. Capsule thickening and increased collagen type I were also observed. There was a significant decrease in Vv, Sv, and Nv of zona fasciculata nuclei in group S compared to group A. The results indicate that aging induces significant morphoquantitative changes in the adrenal gland, which could contribute to the decrease in glucocorticoid production and alterations in aldosterone and cortisol secretion observed in senescence. Understanding these alterations is crucial to developing interventions that mitigate the adverse effects of aging on the endocrine system.


El envejecimiento es un proceso biológico inevitable que afecta la función de todos los órganos, incluida la glándula suprarrenal, fundamental para la producción de hormonas esteroides que regulan el metabolismo, la respuesta al estrés y la activación inmunológica. Comprender cómo el envejecimiento afecta la morfología de esta glándula es crucial para desarrollar intervenciones que mitiguen sus efectos adversos. Así, el objetivo de este estudio fue describir las alteraciones morfocuantitativas de la glándula suprarrenal en ratas Sprague Dawley senescentes comparadas con ratas adultas. Se utilizaron 12 ratas macho, divididas en dos grupos: 6 ratas adultas de 6 meses de edad (grupo A) y 6 ratas senescentes de 36 meses de edad (grupo S). Se realizaron estudios histopatológicos, cuantificación de fibras de colágeno tipos I y III y análisis estereológicos para determinar la densidad de volumen (Vv), de superficie (Sv) y de número (Nv) de los núcleos de las células de la zona fasciculada. El tejido de la glándula suprarrenal del grupo S presentó displasia, metaplasia, acumulación de grasa intracelular, fibrosis, dilatación de vasos sanguíneos y mayor presencia de células apoptósicas. También se observó un engrosamiento de la cápsula y un incremento del colágeno tipo I. Hubo una disminución significativa en Vv, Sv y Nv de los núcleos de la zona fasciculada en el grupo S en comparación con el grupo A. Los resultados indican que el envejecimiento induce cambios morfocuantitativos significativos en la glándula suprarrenal, lo que podría contribuir a la disminución en la producción de glucocorticoides y alteraciones en la secreción de aldosterona y cortisol observadas en la senescencia. Comprender estas alteraciones es crucial para desarrollar intervenciones que mitiguen los efectos adversos del envejecimiento en el sistema endocrino.


Subject(s)
Animals , Male , Rats , Aging , Adrenal Glands/pathology , Fibrosis , Rats, Sprague-Dawley , Fibrillar Collagens/analysis , Metaplasia
4.
Int. j interdiscip. dent. (Print) ; 17(2): 77-80, ago. 2024. ilus, tab
Article in English | LILACS | ID: biblio-1569238

ABSTRACT

Objective: To evaluate the effect of melatonin as a protective treatment for the tongue in irradiated rats. Materials and Methods: Male Sprague Dawley rats were subjected to a single session of 50 Gy radiation and treated with melatonin 30 minutes before and after the radiotherapy session. A clinical evaluation was carried out a week and a half, third- and sixth-week post-treatment; finally, a tongue biopsy was taken for a histopathological study in the third and sixth weeks after radiation. Results: Clinical evaluation shows a clear trend, that preventive administration of melatonin could facilitate the recovery of mucosal tissue after radiation. Additionally, cellular infiltrate was 40% fewer in the melatonin-treated group compared to the control, as well as the number of the congested vessel were fewer. Conclusion: These findings showed for the first time the preventive role of melatonin in the tongue mucosa reducing the changes associated with mucositis, inflammatory infiltrate, and congestive blood vessels.


Subject(s)
Animals , Male , Rats , Radiotherapy/adverse effects , Stomatitis/drug therapy , Melatonin/therapeutic use , Radiation Protection , Stomatitis/etiology , Stomatitis/pathology , Tongue/radiation effects , Tongue Diseases/etiology , Tongue Diseases/pathology , Tongue Diseases/drug therapy , Rats, Sprague-Dawley , Models, Animal , Mouth Mucosa/radiation effects
5.
Int. j. morphol ; 42(3): 607-613, jun. 2024. ilus, tab, graf
Article in English | LILACS | ID: biblio-1564594

ABSTRACT

SUMMARY: Binge drinking in adolescents has a negative effect on the developing skeleton and the attainment of peak bone mass. Our study aimed to examine the effect of binge drinking on the growth and functional integrity of the adolescent Sprague Dawley rat mandible and to determine if a dosage of 1.5 g/kg is sufficient to produce a binge-model of consumption. A total of eight 7-week-old adolescent (male) Sprague Dawley rats were randomly placed into 4 groups with two rats each: 1-week alcohol-exposed rats, 1-week pair- fed control rats, 4-week alcohol-exposed rats and 4-week pair-fed control rats. The alcohol exposed groups were administered a single daily dose via oral gavage of 1.5 g/kg of 20 % alcohol 3 days a week (alternate days) for 7 or 28 days. The pair-fed control groups were administered a caloric equivalent dose of maltose dextrin via oral gavage on the same days as the alcohol-exposed rats. The one-week alcohol exposed, and control rats were terminated on day 7 and the four-week alcohol exposed and control rats on day 28. The mandibles were dissected out and osteometric measurements determined using a digital vernier caliper. Bones were scanned using a 3D-microCT scanner (Nikon XTH 255L). Biomechanical tests were done using a Shimadzu universal testing machine. Differences observed were regarding mandibular osteometry, which showed a reduced height in the central portion of the alveolar bone (Al'-Me), and an increase in the height of the condylar head (Cd-Ag) in the 1-week alcohol-exposed rats when compared to the 1-week pair-fed control rats. No other differences were noted. Lack of significant changes seen between the alcohol and pair-fed control groups in both acute binge and chronic binge exposed rats is likely due to the low dose of alcohol administered to the rats in the study thus a higher dose is proposed.


El consumo excesivo de alcohol en adolescentes tiene un efecto negativo en el desarrollo del esqueleto y en la consecución de la masa ósea máxima. Nuestro estudio tuvo como objetivo examinar el efecto del consumo excesivo de alcohol sobre el crecimiento y la integridad funcional de la mandíbula de la rata adolescente Sprague Dawley y determinar si una dosis de 1,5 g/kg es suficiente para producir un modelo de consumo compulsivo. Un total de ocho ratas Sprague Dawley adolescentes (machos) de 7 semanas de edad se colocaron aleatoriamente en 4 grupos con dos ratas cada uno: ratas expuestas al alcohol durante 1 semana, ratas de control alimentadas en parejas durante 1 semana, ratas expuestas al alcohol durante 4 semanas, y ratas de control alimentadas en parejas durante 4 semanas. A los grupos expuestos al alcohol se les administró una dosis única diaria mediante sonda oral de 1,5 g/kg de alcohol al 20 % 3 días a la semana (días alternos) durante 7 o 28 días. A los grupos de control alimentados por parejas se les administró una dosis calórica equivalente de maltosa dextrina mediante sonda oral los mismos días que a las ratas expuestas al alcohol. Las ratas expuestas al alcohol durante una semana, las ratas de control al día 7, las ratas expuestas al alcohol durante cuatro semanas y las ratas de control al día 28. Se diseccionaron las mandíbulas y se determinaron las mediciones osteométricas utilizando un calibre vernier digital. Los huesos se escanearon utilizando un escáner 3D-microCT (Nikon XTH 255L). Las pruebas biomecánicas se realizaron utilizando una máquina de pruebas universal Shimadzu. Las diferencias observadas se relacionaron con la osteometría mandibular, que mostró una altura reducida en la porción central del hueso alveolar (Al'-Me) y un aumento en la altura de la cabeza condilar (Cd-Ag) en las ratas expuestas al alcohol durante una semana, en comparación con las ratas control alimentadas en parejas durante una semana. No se observaron otras diferencias. La falta de diferencias significativas entre los grupos de alcohol y de control alimentados en parejas expuestas a ebriedad aguda y ebriedad crónica, probablemente se deba a la baja dosis de alcohol administrada a las ratas en el estudio, por lo que se propone una dosis más alta.


Subject(s)
Animals , Male , Rats , Ethanol/administration & dosage , Binge Drinking , Mandible/drug effects , Tensile Strength , Rats, Sprague-Dawley , Blood Alcohol Content , Mandible/anatomy & histology
6.
Int. j. morphol ; 42(3): 647-662, jun. 2024. ilus, tab
Article in English | LILACS | ID: biblio-1564610

ABSTRACT

SUMMARY: The study explores the relationship between chronic exposure to fine particulate matter (PM2.5), sourced from wood smoke, and the histological structure and endocrine function of the uterus in nulliparous adult rats. It assesses potential structural changes in the uterus that could impact reproductive health, viewing PM2.5 exposure as a possible risk factor. A controlled experiment was conducted in a city known for high air pollution levels, exposing rats to filtered and unfiltered air conditions, thus mimicking human PM2.5 exposure. Histological findings indicated a significant increase in collagen density and uterine wall thickness in PM2.5 exposed subjects, suggesting a reproductive function risk. However, no significant differences were observed in progesterone and estradiol hormone levels, pointing to the complex relationship between PM2.5 exposure and its endocrine impact, and emphasizing the need for further studies for a deeper understanding. This work highlights the importance of thoroughly investigating the long-term effects of PM2.5 pollution on reproductive health, underlining the significance of considering environmental exposure as a critical factor in reproductive health research.


El estudio explora la relación entre la exposición crónica a partículas finas (PM2,5), procedentes del humo de leña, y la estructura histológica y la función endocrina del útero en ratas adultas nulíparas. Evalúa posibles cambios estructurales en el útero que podrían afectar la salud reproductiva, considerando la exposición a PM2,5 como un posible factor de riesgo. Se llevó a cabo un experimento controlado en una ciudad conocida por sus altos niveles de contaminación del aire, exponiendo ratas a condiciones de aire filtrado y sin filtrar, imitando así la exposición humana a PM2,5. Los hallazgos histológicos indicaron un aumento significativo en la densidad del colágeno y el grosor de la pared uterina en sujetos expuestos a PM2,5, lo que sugiere un riesgo para la función reproductiva. Sin embargo, no se observaron diferencias significativas en los niveles de las hormonas progesterona y estradiol, lo que apunta a la compleja relación entre la exposición a PM2,5 y su impacto endocrino, y enfatiza la necesidad de realizar más estudios para una comprensión más profunda. Este trabajo destaca la importancia de investigar a fondo los efectos a largo plazo de la contaminación por PM2,5 en la salud reproductiva, subrayando la importancia de considerar la exposición ambiental como un factor crítico en la investigación de la salud reproductiva.


Subject(s)
Animals , Female , Rats , Smoke/adverse effects , Uterus/drug effects , Wood , Rats, Sprague-Dawley , Air Pollutants/toxicity , Air Pollution , Particulate Matter/toxicity , Genitalia, Female/drug effects
7.
Int. j. morphol ; 42(2): 332-340, abr. 2024. ilus
Article in English | LILACS | ID: biblio-1558131

ABSTRACT

SUMMARY: Systemic inflammatory response syndrome (SIRS) is a potentially fatal reaction to various forms of tissue damage and infections that cause damage to various organs. Furthermore, the brain is damaged earlier than other organs, resulting in diffuse brain dysfunction. The central clinical symptom of SIRS is delirium and emotional changes are involved in disease development. Although the amygdala is known to play a major role, the mechanisms underlying emotional changes in the early stages of SIRS have not been elucidated. Therefore, changes to dopamine levels in the amygdala were observed using an in vivo model of lipopolysaccharide (LPS)- induced SIRS to clarify the biochemical mechanisms activated in the early stages of SIRS. Extracellular dopamine was collected from the amygdala of free moving rats via microdialysis and then analyzed by high-performance liquid chromatography. In addition, emotional changes were assessed with the open field and sucrose preference tests. In the LPS group, dopamine release in the amygdala increased remarkably immediately after LPS administration, peaking at 120 min. Thereafter, dopamine release temporarily decreased, but then significantly increased again after 180 min. The present results suggest that diffuse brain dysfunction in the early stages of SIRS may involve altered dopamine levels in the amygdala.


El síndrome de respuesta inflamatoria sistémica (SRIS) es una reacción potencialmente fatal a diversas formas de daño tisular e infecciones que causan injuria a varios órganos. Además, el cerebro se daña antes que otros órganos, lo que provoca una disfunción cerebral difusa. El síntoma clínico central del SIRS es el delirio y los cambios emocionales están involucrados en el desarrollo de la enfermedad. Aunque se sabe que la amígdala desempeña un papel importante, no se han dilucidado los mecanismos que subyacen a los cambios emocionales en las primeras etapas del SRIS. Por lo tanto, en el estudio se provocaron cambios en los niveles de dopamina en la amígdala utilizando un modelo in vivo de SRIS inducido por lipopolisacáridos (LPS) para dilucidar los mecanismos bioquímicos activados en las primeras etapas del SRIS. La dopamina extracelular se recogió de la amígdala de ratas en movimiento libre mediante microdiálisis y luego se analizó mediante cromatografía líquida de alta resolución. Además, se evaluaron los cambios emocionales con las pruebas de campo abierto y de preferencia de sacarosa. En el grupo de LPS, la liberación de dopamina en la amígdala aumentó de manera notable inmediatamente después de la administración de LPS, alcanzando un máximo a los 120 minutos. A partir de entonces, la liberación de dopamina disminuyó temporalmente, pero luego volvió a aumentar significativamente después de 180 min. Los resultadosactuales sugieren que la disfunción cerebral difusa en las primeras etapas del SIRS puede implicar niveles alterados de dopamina en la amígdala.


Subject(s)
Animals , Male , Rats , Dopamine , Systemic Inflammatory Response Syndrome , Amygdala , Lipopolysaccharides/toxicity , Cytokines , Rats, Sprague-Dawley , Systemic Inflammatory Response Syndrome/chemically induced
8.
Int. j. morphol ; 42(2): 452-457, abr. 2024. ilus, tab
Article in English | LILACS | ID: biblio-1558140

ABSTRACT

SUMMARY: Excessive alcohol consumption adversely affects bone metabolism, thus resulting in reduced bone length, density, and strength. Moreover, these deficits in bone density and strength are likely to increase the risk of fragility fractures and the early onset of osteoporosis. While excessive alcohol consumption is an established risk factor for osteoporotic fractures, there remains a dearth of information in literature about bone effects of binge alcohol consumption in adolescents. Therefore, our study aimed to examine the effects of acute binge alcohol consumption on the adolescent bone micro-architecture and tensile strength. Twelve male Sprague Dawley rats aged 7 weeks were randomly placed in 2 groups: alcohol (n =6), receiving alcohol (3g/kg) and pair-fed control (n = 6), receiving an isocaloric equivalent of maltose dextrin via oral gavage for 3 days in one week (on alternative days). The femora were dissected and scanned using a Micro-Focus X-ray Computed Tomography (3D-µCT). Following reconstruction, trabecular morphometry was assessed in both the proximal and distal epiphysis, using a Volume Graphics Studio® software. A three-point bending test was employed to examine the effect of alcohol on the tensile strength of the bone. Results showed trabeculae parameters to be affected in the distal epiphysis of the femur, while in the proximal epiphysis it remained unaffected. Tensile strength parameters were also not affected by the consumption of alcohol. These findings may suggest that acute binge alcohol consumption has detrimental effects on the bone micro-architecture specific to the distal epiphysis.


El consumo excesivo de alcohol afecta negativamente al metabolismo óseo, lo que resulta en una reducción de la longitud, densidad y resistencia de los huesos. Además, es probable que estos déficits en la densidad y la fuerza ósea aumenten el riesgo de fracturas por fragilidad y la aparición temprana de osteoporosis. Si bien el consumo excesivo de alcohol es un factor de riesgo establecido para las fracturas osteoporóticas, existe escasa información en la literatura sobre los efectos óseos del consumo excesivo de alcohol en adolescentes. Por lo tanto, nuestro estudio tuvo como objetivo examinar los efectos del consumo excesivo de alcohol en la microarquitectura ósea y la resistencia a la tracción e n ratas adolescentes. Doce ratas macho Sprague Dawley de 7 semanas de edad se colocaron aleatoriamente en 2 grupos: alcohol (n = 6), que recibieron alcohol (3 g/kg) y control (n = 6), que recibieron un equivalente isocalórico de maltosa dextrina mediante sonda oral, durante 3 días en una semana (en días alternos). Los fémures se diseccionaron y escanearon mediante una tomografía computarizada de rayos X con microenfoque (3D-mCT). Después de la reconstrucción, se evaluó la morfometría trabecular tanto en la epífisis proximal como en la distal, utilizando un software Volume Graphics Studio®. Se empleó una prueba de flexión de tres puntos para examinar el efecto del alcohol sobre la resistencia a la tracción del hueso. Los resultados mostraron que los parámetros de las trabéculas se vieron afectados en la epífisis distal del fémur, mientras que en la epífisis proximal no se observaron afectados. Los parámetros de resistencia a la tracción tampoco se vieron afectados por el consumo de alcohol. Estos hallazgos pueden sugerir que el consumo excesivo de alcohol tiene efectos perjudiciales sobre la microarquitectura ósea específica de la epífisis distal del hueso.


Subject(s)
Animals , Rats , Alcohol Drinking/adverse effects , Ethanol/toxicity , Femur/drug effects , Cancellous Bone/drug effects , Rats, Sprague-Dawley , Ethanol/blood , Blood Alcohol Content
9.
Int. j. morphol ; 42(2): 470-478, abr. 2024. ilus
Article in English | LILACS | ID: biblio-1558149

ABSTRACT

SUMMARY: We evaluated the role and mechanism of acteoside in the regulation of memory impairment induced by chronic unpredictable mild stress (CUMS). CUMS was used to induce depression in rats and the successful establishment of CUMS model were verified by forced swimming test and sucrose preference test. The Y-maze test and novel object recognition test assessed memory functions. The structural changes in the cortex and hippocampus were observed by hematoxylin and eosin (HE) staining. Immunofluorescence staining and western blotting determined the protein levels. Y-maze test and novel object recognition test showed that there was memory performance impairment in rats of CUMS group, which was improved by the acteoside treatment. HE staining showed that CUMS exposure damaged the structure in the cortex and hippocampus, while the acteoside treatment alleviated the structural changes. Compared with the control group, the levels of BNDF and CREB in the cortex and hippocampus of the CUMS group were significantly decreased. Acteoside significantly reversed the expressions of these proteins in CUMS rats. Meanwhile, compared with the control group, the levels of p-mTOR and p- P70S6K in the cortex and hippocampus of the CUMS group were significantly increased, and these changes were significantly reversed by acteoside. Nevertheless, the effect of acteoside on mTOR signaling was markedly blocked by rapamycin, a specific inhibitor of mTOR signaling. Acteoside can attenuate memory impairment and ameliorate neuronal damage and synaptic plasticity in depression rats probably via inhibiting the mTOR signaling pathway. Acteoside may serve as a novel reagent for the prevention of depression.


Evaluamos el papel y el mecanismo del acteoside en la regulación del deterioro de la memoria inducido por estrés leve crónico impredecible (ELCI). Se utilizó ELCI para inducir depresión en ratas y el establecimiento exitoso del modelo ELCI se verificó mediante una prueba de natación forzada y una prueba de preferencia de sacarosa. La prueba del laberinto en Y y la prueba de reconocimiento de objetos novedosos evaluaron las funciones de la memoria. Los cambios estructurales en la corteza y el hipocampo se observaron mediante tinción con hematoxilina y eosina (HE). La tinción por inmunofluorescencia y la transferencia Western determinaron los niveles de proteína. La prueba del laberinto en Y y la prueba de reconocimiento de objetos novedosos mostraron que había un deterioro del rendimiento de la memoria en ratas del grupo ELCI, que mejoró con el tratamiento con acteósidos. La tinción con HE mostró que la exposición a ELCI dañó la estructura de la corteza y el hipocampo, mientras que el tratamiento con actósidos alivió los cambios estructurales. En comparación con el grupo de control, los niveles de BNDF y CREB en la corteza y el hipocampo del grupo ELCI disminuyeron significativamente. Acteoside revirtió significativamente las expresiones de estas proteínas en ratas ELCI. Mientras tanto, en comparación con el grupo control, los niveles de p-mTOR y p-P70S6K en la corteza y el hipocampo del grupo ELCI aumentaron significativamente, y estos cambios fueron revertidos significativamente ELCI por el acteoside. Sin embargo, el efecto del acteoside sobre la señalización de mTOR fue notablemente bloqueado por la rapamicina, un inhibidor específico de la señalización de mTOR. El acteoside puede atenuar el deterioro de la memoria y mejorar el daño neuronal y la plasticidad sináptica en ratas con depresión, probablemente mediante la inhibición de la vía de señalización mTOR. Acteoside puede servir como un reactivo novedoso para la prevención de la depresión.


Subject(s)
Animals , Rats , Depression/drug therapy , Polyphenols/administration & dosage , Glucosides/administration & dosage , Memory Disorders/drug therapy , Stress, Psychological/complications , Blotting, Western , Fluorescent Antibody Technique , Rats, Sprague-Dawley , Maze Learning , Recognition, Psychology/drug effects , Disease Models, Animal , TOR Serine-Threonine Kinases/antagonists & inhibitors , Polyphenols/therapeutic use , Behavior Rating Scale , MTOR Inhibitors , Glucosides/therapeutic use , Neuronal Plasticity/drug effects , Neurons
10.
Int. j. morphol ; 42(1): 205-215, feb. 2024. ilus, tab
Article in English | LILACS | ID: biblio-1528814

ABSTRACT

SUMMARY: This study assessed the effects of Acacia Senegal (AS) combined with insulin on Na+/K+-ATPase (NKA) activity and mRNA expression, serum glucose, renal function, and oxidative stress in a rat model of diabetic nephropathy (DN). Sixty rats were equally divided into six groups: normal control, normal+AS, diabetic (DM), DM+insulin, DM+AS, and DM+insulin+AS groups. Diabetes mellitus (type 1) was induced by a single injection of streptozotocin (65 mg/kg), and insulin and AS treatments were carried until rats were culled at the end of week 12. Serum glucose and creatinine levels, hemoglobin A1c (HbA1c) were measured. Renal homogenate levels of NKA activity and gene expression, malondialdehyde, superoxide dismutase (SOD), catalase and reduced glutathione (GSH) were evaluated as well as kidney tissue histology and ultrastructure. Diabetes caused glomerular damage and modulation of blood and tissue levels of creatinine, glucose, HbA1c, malondialdehyde, NKA activity and gene expression, SOD, catalase and GSH, which were significantly (p<0.05) treated with AS, insulin, and insulin plus AS. However, AS+insulin treatments were more effective. In conclusion, combined administration of AS with insulin to rats with DN decreased NKA activity and gene expression as well as oxidative stress, and improved glycemic state and renal structure and function.


Este estudio evaluó los efectos de Acacia senegal (AS) combinada con insulina sobre la actividad Na+/K+- ATPasa (NKA) y la expresión de ARNm, la glucosa sérica, la función renal y el estrés oxidativo en un modelo de nefropatía diabética (ND) en ratas. Sesenta ratas se dividieron equitativamente en seis grupos: control normal, normal+AS, diabética (DM), DM+insulina, DM+AS y DM+insulina+AS. La diabetes mellitus (tipo 1) se indujo mediante una única inyección de estreptozotocina (65 mg/kg), y los tratamientos con insulina y AS se llevaron a cabo hasta que las ratas fueron sacrificadas al final de la semana 12. Se midieron niveles séricos de glucosa y creatinina, hemoglobina A1c (HbA1c). Se evaluaron los niveles de homogeneizado renal de actividad NKA y expresión génica, malondialdehído, superóxido dismutasa (SOD), catalasa y glutatión reducido (GSH), así como la histología y ultraestructura del tejido renal. La diabetes causó daño glomerular y modulación de los niveles sanguíneos y tisulares de creatinina, glucosa, HbA1c, malondialdehído, actividad y expresión génica de NKA, SOD, catalasa y GSH, los cuales fueron tratados significativamente (p<0,05) con AS, insulina e insulina más AS. Sin embargo, los tratamientos con AS+insulina fueron más efectivos. En conclusión, la administración combinada de AS con insulina a ratas con DN disminuyó la actividad de NKA y la expresión genética, así como el estrés oxidativo, y mejoró el estado glucémico y la estructura y función renal.


Subject(s)
Animals , Male , Rats , Plant Extracts/administration & dosage , Sodium-Potassium-Exchanging ATPase/drug effects , Diabetic Nephropathies/drug therapy , Acacia/chemistry , Superoxide Dismutase , Glycated Hemoglobin/analysis , Plant Extracts/pharmacology , Gene Expression , Rats, Sprague-Dawley , Sodium-Potassium-Exchanging ATPase/genetics , Oxidative Stress , Microscopy, Electron, Transmission , Disease Models, Animal , Drug Therapy, Combination , Glycemic Control , Insulin/administration & dosage , Kidney/drug effects , Malondialdehyde
11.
Chin. j. integr. med ; Chin. j. integr. med;(12): 152-162, 2024.
Article in English | WPRIM | ID: wpr-1010329

ABSTRACT

OBJECTIVE@#To investigate whether electroacupuncture (EA) at sensitized acupoints could reduce sympathetic-sensory coupling (SSC) and neurogenic inflammatory response by interfering with 5-hydroxytryptamine (5-HT)ergic neural pathways to relieve colitis and somatic referred pain, and explore the underlying mechanisms.@*METHODS@#Rats were treated with 5% dextran sodium sulfate (DSS) solution for 7 days to establish a colitis model. Twelve rats were randomly divided into the control and model groups according to a random number table (n=6). According to the "Research on Rat Acupoint Atlas", sensitized acupoints and non-sensitized acupoints were determined. Rats were randomly divided into the control, model, Zusanli-EA (ST 36), Dachangshu-EA (BL 25), and Xinshu (BL 15) groups (n=6), as well as the control, model, EA, and EA + GR113808 (a 5-HT inhibitor) groups (n=6). The rats in the control group received no treatment. Acupuncture was administered on 2 days after modeling using the stimulation pavameters: 1 mA, 2 Hz, for 30 min, with sparse and dense waves, for 14 consecutive days. GR113808 was injected into the tail vein at 5 mg/kg before EA for 10 min for 7 consecutive days. Mechanical sensitivity was assessed with von Frey filaments. Body weight and disease activity index (DAI) scores of rats were determined. Hematoxylin and eosin staining was performed to observe colon histopathology. SSC was analyzed by immunofluorescence staining. Immunohistochemical staining was performed to detect 5-HT and substance P (SP) expressions. The calcitonin gene-related peptide (CGRP) in skin tissue and tyrosine hydroxylase (TH) protein levels in DRG were detected by Western blot. The levels of hyaluronic acid (HA), bradykinin (BK), prostaglandin I2 (PGI2) in skin tissue, 5-HT, tryptophan hydroxylase 1 (TPH1), serotonin transporters (SERT), 5-HT 3 receptor (5-HT3R), and 5-HT 4 receptor (5-HT4R) in colon tissue were measured by enzyme-linked immunosorbent assay (ELISA).@*RESULTS@#BL 25 and ST 36 acupoints were determined as sensitized acupoints, and BL 15 acupoint was used as a non-sensitized acupoint. EA at sensitized acupoints improved the DAI score, increased mechanical withdrawal thresholds, and alleviated colonic pathological damage of rats. EA at sensitized acupoints reduced SSC structures and decreased TH and CGRP expression levels (P<0.05). Furthermore, EA at sensitized acupoints reduced BK, PGI2, 5-HT, 5-HT3R and TPH1 levels, and increased HA, 5-HT4R and SERT levels in colitis rats (P<0.05). GR113808 treatment diminished the protective effect of EA at sensitized acupoints in colitis rats (P<0.05).@*CONCLUSION@#EA at sensitized acupoints alleviated DSS-induced somatic referred pain in colitis rats by interfering with 5-HTergic neural pathway, and reducing SSC inflammatory response.


Subject(s)
Rats , Animals , Electroacupuncture , Rats, Sprague-Dawley , Serotonin , Acupuncture Points , Pain, Referred , Calcitonin Gene-Related Peptide , Signal Transduction , Colitis/therapy , Indoles , Sulfonamides
12.
Chin. j. integr. med ; Chin. j. integr. med;(12): 251-259, 2024.
Article in English | WPRIM | ID: wpr-1010332

ABSTRACT

OBJECTIVE@#To explore the mechanism of electroacupuncture (EA) in promoting recovery of the facial function with the involvement of autophagy, glial cell line-derived neurotrophic factor (GDNF), and phosphatidylinositol-3-kinase (PI3K)/mammalian target of rapamycin (mTOR) signaling pathway.@*METHODS@#Seventy-two male Sprague-Dawley rats were randomly allocated into the control, sham-operated, facial nerve injury (FNI), EA, EA+3-methyladenine (3-MA), and EA+GDNF antagonist groups using a random number table, with 12 rats in each group. An FNI rat model was established with facial nerve crushing method. EA intervention was conducted at Dicang (ST 4), Jiache (ST 6), Yifeng (SJ 17), and Hegu (LI 4) acupoints for 2 weeks. The Simone's 10-Point Scale was utilized to monitor the recovery of facial function. The histopathological evaluation of facial nerves was performed using hematoxylin-eosin (HE) staining. The levels of Beclin-1, light chain 3 (LC3), and P62 were detected by immunohistochemistry (IHC), immunofluorescence, and reverse transcription-polymerase chain reaction, respectively. Additionally, IHC was also used to detect the levels of GDNF, Rai, PI3K, and mTOR.@*RESULTS@#The facial functional scores were significantly increased in the EA group than the FNI group (P<0.05 or P<0.01). HE staining showed nerve axons and myelin sheaths, which were destroyed immediately after the injury, were recovered with EA treatment. The expressions of Beclin-1 and LC3 were significantly elevated and the expression of P62 was markedly reduced in FNI rats (P<0.01); however, EA treatment reversed these abnormal changes (P<0.01). Meanwhile, EA stimulation significantly increased the levels of GDNF, Rai, PI3K, and mTOR (P<0.01). After exogenous administration with autophagy inhibitor 3-MA or GDNF antagonist, the repair effect of EA on facial function was attenuated (P<0.05 or P<0.01).@*CONCLUSIONS@#EA could promote the recovery of facial function and repair the facial nerve damages in a rat model of FNI. EA may exert this neuroreparative effect through mediating the release of GDNF, activating the PI3K/mTOR signaling pathway, and further regulating the autophagy of facial nerves.


Subject(s)
Rats , Male , Animals , Rats, Sprague-Dawley , Electroacupuncture , Phosphatidylinositol 3-Kinase/metabolism , Facial Nerve Injuries/therapy , Phosphatidylinositol 3-Kinases/metabolism , Beclin-1 , Glial Cell Line-Derived Neurotrophic Factor , Signal Transduction , TOR Serine-Threonine Kinases/metabolism , Autophagy , Mammals/metabolism
13.
Article in Chinese | WPRIM | ID: wpr-1009112

ABSTRACT

OBJECTIVE@#To investigate the effects and underlying mechanisms of VX765 on osteoarthritis (OA) and chondrocytes inflammation in rats.@*METHODS@#Chondrocytes were isolated from the knee joints of 4-week-old Sprague Dawley (SD) rats. The third-generation cells were subjected to cell counting kit 8 (CCK-8) analysis to assess the impact of various concentrations (0, 1, 5, 10, 20, 50, 100 μmol/L) of VX765 on rat chondrocyte activity. An in vitro lipopolysaccharide (LPS) induced cell inflammation model was employed, dividing cells into control group, LPS group, VX765 concentration 1 group and VX765 concentration 2 group without obvious cytotoxicity. Western blot, real-time fluorescence quantitative PCR, and ELISA were conducted to measure the expression levels of inflammatory factors-transforming growth factor β 1 (TGF-β 1), interleukin 6 (IL-6), and tumor necrosis factor α (TNF-α). Additionally, Western blot and immunofluorescence staining were employed to assess the expressions of nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase 1 (HO-1). Thirty-two SD rats were randomly assigned to sham surgery group (group A), OA group (group B), OA+VX765 (50 mg/kg) group (group C), and OA+VX765 (100 mg/kg) group (group D), with 8 rats in each group. Group A underwent a sham operation with a medial incision, while groups B to D underwent additional transverse incisions to the medial collateral ligament and anterior cruciate ligament, with removal of the medial meniscus. One week post-surgery, groups C and D were orally administered 50 mg/kg and 100 mg/kg VX765, respectively, while groups A and B received an equivalent volume of saline. Histopathological examination using HE and safranin-fast green staining was performed, and Mankin scoring was utilized for evaluation. Immunohistochemical staining technique was employed to analyze the expressions of matrix metalloproteinase 13 (MMP-13) and collagen type Ⅱ.@*RESULTS@#The CCK-8 assay indicated a significant decrease in cell viability at VX765 concentrations exceeding 10 μmol/L ( P<0.05), so 4 μmol/L and 8 μmol/L VX765 without obvious cytotoxicity were selected for subsequent experiments. Following LPS induction, the expressions of TGF-β 1, IL-6, and TNF-α in cells significantly increased when compared with the control group ( P<0.05). However, intervention with 4 μmol/L and 8 μmol/L VX765 led to a significant decrease in expression compared to the LPS group ( P<0.05). Western blot and immunofluorescence staining demonstrated a significant upregulation of Nrf2 pathway-related molecules Nrf2 and HO-1 protein expressions by VX765 ( P<0.05), indicating Nrf2 pathway activation. Histopathological examination of rat knee joint tissues and immunohistochemical staining revealed that, compared to group B, treatment with VX765 in groups C and D improved joint structural damage in rat OA, alleviated inflammatory reactions, downregulated MMP-13 expression, and increased collagen type Ⅱ expression.@*CONCLUSION@#VX765 can improve rat OA and reduce chondrocyte inflammation, possibly through the activation of the Nrf2 pathway.


Subject(s)
Rats , Animals , Chondrocytes/metabolism , Matrix Metalloproteinase 13/metabolism , Rats, Sprague-Dawley , Tumor Necrosis Factor-alpha/metabolism , Collagen Type II/metabolism , Interleukin-6 , Lipopolysaccharides/pharmacology , NF-E2-Related Factor 2/pharmacology , Inflammation/drug therapy , Osteoarthritis/metabolism , Transforming Growth Factor beta1/metabolism , Dipeptides , para-Aminobenzoates
14.
Article in Chinese | WPRIM | ID: wpr-1009224

ABSTRACT

OBJECTIVE@#To explore the effect of shikonin on the recovery of nerve function after acute spinal cord injury(SCI) in rats.@*METHODS@#96 male Sprague-Dawley(SD)rats were divided into 4 groups randomly:sham operation group (Group A), sham operation+shikonin group (Group B), SCI+ DMSO(Group C), SCI+shikonin group (Group D).The acute SCI model of rats was made by clamp method in groups C and D . After subdural catheterization, no drug was given in group A. rats in groups B and D were injected with 100 mg·kg-1 of shikonin through catheter 30 min after modeling, and rats in group C were given with the same amount of DMSO, once a day until the time point of collection tissue. Basso-Beattie-Bresnahan(BBB) scores were performed on 8 rats in each group at 6, 12, and 3 d after moneling, and oblique plate tests were performed on 1, 3, 7 and 14 d after modeling, and then spinal cord tissues were collected. Eight rats were intraperitoneally injected with propidine iodide(PI) 1 h before sacrificed to detection PI positive cells at 24 h in each group. Eight rats were sacrificed in each group at 24 h after modeling, the spinal cord injury was observed by HE staining.The Nissl staining was used to observe survivor number of nerve cells. Western-blot technique was used to detect the expression levels of Bcl-2 protein and apoptosis related protein RIPK1.@*RESULTS@#After modeling, BBB scores were normal in group A and B, but in group C and D were significantly higher than those in group A and B. And the scores in group D were higher than those in group C in each time point (P<0.05). At 12 h after modeling, the PI red stained cells in group D were significantly reduced compared with that in group C, and the disintegration of neurons was alleviated(P<0.05). HE and Nissl staining showed nerve cells with normal morphology in group A and B at 24h after operation. The degree of SCI and the number of neuronal survival in group D were better than those in group C, the difference was statistically significant at 24h (P<0.05). The expression of Bcl-2 and RIPK1 proteins was very low in group A and B;The expression of RIPK1 was significantly increased in Group C and decreased in Group D, with a statistically significant difference (P<0.05);The expression of Bcl-2 protein in group D was significantly higher than that in group C (P<0.05).@*CONCLUSION@#Shikonin can alleviate the pathological changes after acute SCI in rats, improve the behavioral score, and promote the recovery of spinal nerve function. The specific mechanism may be related to the inhibition of TNFR/RIPK1 signaling pathway mediated necrotic apoptosis.


Subject(s)
Animals , Male , Rats , Dimethyl Sulfoxide/metabolism , Naphthoquinones , Proto-Oncogene Proteins c-bcl-2/metabolism , Rats, Sprague-Dawley , Spinal Cord/metabolism , Spinal Cord Injuries/metabolism , Receptors, Tumor Necrosis Factor/metabolism , Receptor-Interacting Protein Serine-Threonine Kinases/metabolism
15.
Article in Chinese | WPRIM | ID: wpr-1009225

ABSTRACT

OBJECTIVE@#To explore effect of nerve growth factor (NGF) antibody on knee osteoarthritis (KOA) pain model was evaluated by in vitro model.@*METHODS@#Thirty male SPF rats aged 28-week-old were divided into blank group (10 rats with anesthesia only). The other 20 rats were with monoiodoacetate (MIA) on the right knee joint to establish pain model of OA, and were randomly divided into control group (injected intraperitoneal injection of normal saline) and treatment group (injected anti-NGF) intraperitoneal after successful modeling, and 10 rats in each group. All rats were received retrograde injection of fluorogold (FG) into the right knee joint. Gait was assessed using catwalk gait analysis system before treatment, 1 and 2 weeks after treatment. Three weeks after treatment, right dorsal root ganglia (DRG) were excised on L4-L6 level, immunostained for calcitonin gene-related peptide (CGRP), and the number of DRGS was counted.@*RESULTS@#In terms of gait analysis using cat track system, duty cycle, swing speed and print area ratio in control and treatment group were significantly reduced compared with blank group (P<0.05). Compared with control group, duty cycle and swing speed of treatment group were significantly improved (P<0.05), and there was no significant difference in print area ratio between treatment group and blank group (P>0.05). The number of FG-labeled DRG neurons in control group was significantly higher than that in treatment group and blank group (P<0.05). The expression of CGRP in control group was up-regulated, and differences were statistically significant compared with treatment group (P<0.05).@*CONCLUSION@#Intraperitoneal injection of anti-NGF antibody inhibited gait injury and upregulation of CGRP in DRG neurons. The results suggest that anti-nerve growth factor therapy may be of value in treating knee pain. NGF may be an important target for the treatment of knee OA pain.


Subject(s)
Aged , Animals , Male , Rats , Calcitonin Gene-Related Peptide/metabolism , Disease Models, Animal , Ganglia, Spinal/metabolism , Knee Joint , Nerve Growth Factor/therapeutic use , Osteoarthritis, Knee/drug therapy , Pain/metabolism , Rats, Sprague-Dawley , Antibodies/therapeutic use
16.
Chin. j. traumatol ; Chin. j. traumatol;(6): 18-26, 2024.
Article in English | WPRIM | ID: wpr-1009495

ABSTRACT

PURPOSE@#The incidence of heatstroke (HS) is not particularly high; however, once it occurs, the consequences are serious. It is reported that calcitonin gene-related peptide (CGRP) is protective against brain injury in HS rats, but detailed molecular mechanisms need to be further investigated. In this study, we further explored whether CGRP inhibited neuronal apoptosis in HS rats via protein kinase A (PKA)/p-cAMP response element-binding protein (p-CREB) pathway.@*METHODS@#We established a HS rat model in a pre-warmed artificial climate chamber with a temperature of (35.5 ± 0.5) °C and a relative humidity of 60% ± 5%. Heatstress was stopped once core body temperature reaches above 41 °C. A total of 25 rats were randomly divided into 5 groups with 5 animals each: control group, HS group, HS+CGRP group, HS+CGRP antagonist (CGRP8-37) group, and HS+CGRP+PKA/p-CREB pathway blocker (H89) group. A bolus injection of CGRP was administered to each rat in HS+CGRP group, CGRP8-37 (antagonist of CGRP) in HS+CGRP8-37 group, and CGRP with H89 in HS+CGRP+H89 group. Electroencephalograms were recorded and the serum concentration of S100B, neuron-specific enolase (NSE), neuron apoptosis, activated caspase-3 and CGRP expression, as well as pathological morphology of brain tissue were detected at 2 h, 6 h, and 24 h after HS in vivo. The expression of PKA, p-CREB, and Bcl-2 in rat neurons were also detected at 2 h after HS in vitro. Exogenous CGRP, CGRP8-37, or H89 were used to determine whether CGRP plays a protective role in brain injury via PKA/p-CREB pathway. The unpaired t-test was used between the 2 samples, and the mean ± SD was used for multiple samples. Double-tailed p < 0.05 was considered statistically significant.@*RESULTS@#Electroencephalogram showed significant alteration of θ (54.50 ± 11.51 vs. 31.30 ± 8.71, F = 6.790, p = 0.005) and α wave (16.60 ± 3.21 vs. 35.40 ± 11.28, F = 4.549, p = 0.020) in HS group compared to the control group 2 h after HS. The results of triphosphate gap terminal labeling (TUNEL) showed that the neuronal apoptosis of HS rats was increased in the cortex (9.67 ± 3.16 vs. 1.80 ± 1.10, F = 11.002, p = 0.001) and hippocampus (15.73 ± 8.92 vs. 2.00 ± 1.00, F = 4.089, p = 0.028), the expression of activated caspase-3 was increased in the cortex (61.76 ± 25.13 vs. 19.57 ± 17.88, F = 5.695, p = 0.009) and hippocampus (58.60 ± 23.30 vs. 17.80 ± 17.62, F = 4.628, p = 0.019); meanwhile the expression of serum NSE (5.77 ± 1.78 vs. 2.35 ± 0.56, F = 5.174, p = 0.013) and S100B (2.86 ± 0.69 vs. 1.35 ± 0.34, F = 10.982, p = 0.001) were increased significantly under HS. Exogenous CGRP decreased the concentrations of NSE and S100B, and activated the expression of caspase-3 (0.41 ± 0.09 vs. 0.23 ± 0.04, F = 32.387, p < 0.001) under HS; while CGRP8-37 increased NSE (3.99 ± 0.47 vs. 2.40 ± 0.50, F = 11.991, p = 0.000) and S100B (2.19 ± 0.43 vs. 1.42 ± 0.30, F = 4.078, p = 0.025), and activated the expression caspase-3 (0.79 ± 0.10 vs. 0.23 ± 0.04, F = 32.387, p < 0.001). For the cell experiment, CGRP increased Bcl-2 (2.01 ± 0.73 vs. 2.15 ± 0.74, F = 8.993, p < 0.001), PKA (0.88 ± 0.08 vs. 0.37 ± 0.14, F = 20.370, p < 0.001), and p-CREB (0.87 ± 0.13 vs. 0.29 ± 0.10, F = 16.759, p < 0.001) levels; while H89, a blocker of the PKA/p-CREB pathway reversed the expression.@*CONCLUSIONS@#CGRP can protect against HS-induced neuron apoptosis via PKA/p-CREB pathway and reduce activation of caspase-3 by regulating Bcl-2. Thus CGRP may be a new target for the treatment of brain injury in HS.


Subject(s)
Animals , Rats , Apoptosis , Brain Injuries/pathology , Calcitonin Gene-Related Peptide/metabolism , Caspase 3 , Isoquinolines , Proto-Oncogene Proteins c-bcl-2 , Rats, Sprague-Dawley , Sulfonamides , Heat Stroke/pathology
17.
Zhonghua xinxueguanbing zazhi ; (12): 72-78, 2024.
Article in Chinese | WPRIM | ID: wpr-1045791

ABSTRACT

Objective: To investigate the effects of exosome derived from miR-133a-3p engineered human umbilical cord blood mesenchymal stem cells (ucMSC) on myocardial repair after acute myocardial infarction (AMI) in rats. Methods: UcMSC was amplified and cultured in vitro. Lentiviral carrying miR-133a-3p and negative control vectors were transfected into ucMSC. Exosomes secreted by the transfected ucMSC were named miR-133a-3p-Exo and miR-NC-Exo, respectively. The AMI model of rats was established by ligation of the left anterior descending coronary artery. MiR-133a-3p-Exo or miR-NC-Exo were then injected into the border zone of the infarct area. Cardiac function was assessed by echocardiography after twenty-eight days of intervention, and Masson staining was used to evaluate the area of myocardial fibrosis post-AMI. The myocardial apoptosis after infarction was evaluated by TUNEL staining and the angiogenesis after infarction was evaluated by immunofluorescence staining in the current study. Results: Compared with the miR-NC-Exo group, the left ventricular ejection fraction in the miR-133a-3p-Exo group was significantly increased ((47.4%±9.8%) vs. (64.2%±8.9%), P<0.05). While the myocardial fibrosis area ((31.2%±7.3%) vs. (18.0%±1.5%), P<0.01) and the percentage of apoptotic cardiomyocytes ((25.6%±3.6%) vs. (15.1%±4.4%), P<0.05) was significantly reduced in the miR-133a-Exo group. Besides, the expression of CD31 and α-smooth muscle actin (α-SMA) were also increased significantly in the miR-133a-3p-Exo group compared to the miR-NC-Exo group (CD31: (2.9±0.9) vs. (13.9±2.0), P<0.000 1, α-SMA: (3.5±0.9) vs. (11.0±1.6), P<0.000 1). Conclusion: Exosome derived from miR-133a-3p engineered ucMSC effectively inhibited myocardial apoptosis and promoted angiogenesis, thus improving the cardiac function after myocardial infarction in rats.


Subject(s)
Rats , Humans , Animals , Exosomes/metabolism , Stroke Volume , Rats, Sprague-Dawley , MicroRNAs/genetics , Ventricular Function, Left , Myocardial Infarction/genetics , Cardiomyopathies/metabolism , Fibrosis , Mesenchymal Stem Cells/metabolism , Apoptosis
18.
Zhonghua xinxueguanbing zazhi ; (12): 72-78, 2024.
Article in Chinese | WPRIM | ID: wpr-1046114

ABSTRACT

Objective: To investigate the effects of exosome derived from miR-133a-3p engineered human umbilical cord blood mesenchymal stem cells (ucMSC) on myocardial repair after acute myocardial infarction (AMI) in rats. Methods: UcMSC was amplified and cultured in vitro. Lentiviral carrying miR-133a-3p and negative control vectors were transfected into ucMSC. Exosomes secreted by the transfected ucMSC were named miR-133a-3p-Exo and miR-NC-Exo, respectively. The AMI model of rats was established by ligation of the left anterior descending coronary artery. MiR-133a-3p-Exo or miR-NC-Exo were then injected into the border zone of the infarct area. Cardiac function was assessed by echocardiography after twenty-eight days of intervention, and Masson staining was used to evaluate the area of myocardial fibrosis post-AMI. The myocardial apoptosis after infarction was evaluated by TUNEL staining and the angiogenesis after infarction was evaluated by immunofluorescence staining in the current study. Results: Compared with the miR-NC-Exo group, the left ventricular ejection fraction in the miR-133a-3p-Exo group was significantly increased ((47.4%±9.8%) vs. (64.2%±8.9%), P<0.05). While the myocardial fibrosis area ((31.2%±7.3%) vs. (18.0%±1.5%), P<0.01) and the percentage of apoptotic cardiomyocytes ((25.6%±3.6%) vs. (15.1%±4.4%), P<0.05) was significantly reduced in the miR-133a-Exo group. Besides, the expression of CD31 and α-smooth muscle actin (α-SMA) were also increased significantly in the miR-133a-3p-Exo group compared to the miR-NC-Exo group (CD31: (2.9±0.9) vs. (13.9±2.0), P<0.000 1, α-SMA: (3.5±0.9) vs. (11.0±1.6), P<0.000 1). Conclusion: Exosome derived from miR-133a-3p engineered ucMSC effectively inhibited myocardial apoptosis and promoted angiogenesis, thus improving the cardiac function after myocardial infarction in rats.


Subject(s)
Rats , Humans , Animals , Exosomes/metabolism , Stroke Volume , Rats, Sprague-Dawley , MicroRNAs/genetics , Ventricular Function, Left , Myocardial Infarction/genetics , Cardiomyopathies/metabolism , Fibrosis , Mesenchymal Stem Cells/metabolism , Apoptosis
19.
Braz. j. biol ; 84: e254646, 2024. tab, ilus
Article in English | LILACS, VETINDEX | ID: biblio-1360224

ABSTRACT

Chronic stress (CS) can contribute to dysfunction in several organs including liver and kidney. This study was performed to investigate the changes in serum biochemistry, histological structure, as well as in localization of tyrosine phosphorylated proteins (TyrPho) and Heat shock protein 70 (Hsp-70) in liver and kidney tissues of CS rats induced by two stressors (restrained and force swimming) for 60 consecutive days. Samples of blood, liver, and kidney were collected from adult male Sprague-Dawley rats in each group. Our results showed that serum biochemical parameters including corticosterone, blood sugar, urea nitrogen, creatinine, cholesterol, triglyceride, HDL-C, LDL-C, ALT, AST, alkaline phosphatase in CS group were significantly different from that in normal group in both liver and kidney tissues. Although histological structure was not changed. TyrPho expression was significantly increased in liver lysate but significantly decreased in kidney. Hsp-70 expression in liver increased whereas in kidney decreased. In conclusion, CS can induce changes in liver and kidney functions.


O estresse crônico (SC) pode contribuir para a disfunção em vários órgãos, incluindo fígado e rim. Este estudo foi realizado para investigar as alterações na bioquímica sérica, estrutura histológica, bem como na localização de proteínas tirosina fosforiladas (TyrPho) e proteína de choque térmico 70 (Hsp-70) em tecidos hepáticos e renais de ratos CS induzidas por dois estressores (restrito e natação forçada) por 60 dias consecutivos. Amostras de sangue, fígado e rim foram coletadas de ratos Sprague-Dawley machos adultos em cada grupo. Nossos resultados mostraram que os parâmetros bioquímicos séricos, incluindo corticosterona, glicemia, nitrogênio ureico, creatinina, colesterol, triglicerídeos, HDL-C, LDL-C, ALT, AST, fosfatase alcalina no grupo CS foram significativamente diferentes do grupo normal em ambos os fígados e tecidos renais. Embora a estrutura histológica não tenha sido alterada, a expressão de TyrPho aumentou significativamente no lisado hepático, mas diminuiu significativamente no rim. A expressão de Hsp-70 no fígado aumentou, enquanto que no rim diminuiu. Em conclusão, a CS pode induzir alterações nas funções hepáticas e renais.


Subject(s)
Rats , Stress, Physiological , Rats, Sprague-Dawley , Kidney/anatomy & histology , Liver/anatomy & histology
20.
Int. j. morphol ; 41(6): 1808-1815, dic. 2023. ilus, tab
Article in English | LILACS | ID: biblio-1528773

ABSTRACT

SUMMARY: The R-spondin protein family is a group of proteins that enhance Wnt/b-catenin signaling and have pleiotropic functions in stem cell growth and development. In the literature reviews, there is no histomorphological study showing the localization and distribution of R-spondins in different hypothalamic nuclei. For this reason, the purpose of this study was to determine the localization, distribution characteristics, and densities in the hypothalamic nuclei of neurons expressing Rspo1 and Rspo3 proteins. The free-floating brain sections of the male rats who were not exposed to any treatment were stained with the indirect immunoperoxidase method using the relevant antibodies. As a result of the immunohistochemical studies, it was determined that neurons expressing the Rspo1 protein were found in large numbers in the supraoptic nucleus (SON), the suprachiasmatic nucleus (SCh), anterior paraventricular nucleus, periventricular hypothalamic nucleus (PeV), anterior hypothalamic area, magnocellular preoptic nucleus (MCPO) and the lateral hypothalamic area (LH) from the hypothalamic nuclei, while they were localized in fewer numbers in the arcuate nucleus (ARC). Rspo3 protein expression was found in neurons localized in the hypothalamic nuclei SON, paraventricular nucleus (PVN), PeV, ARC, ventromedial nucleus (VMH), LH, anterior parvicellular nucleus, and zona inserta (ZI). In addition, neurons synthesizing both peptides were found in the cortex and hippocampus regions (H). Rspo1 and 3 proteins are expressed in hypothalamic energy homeostatic areas, thus these proteins may be involved in the regulation of food intake.


La familia de proteínas R-espondina es un grupo de proteínas que mejoran la señalización de Wnt/b-catenina y tienen funciones pleiotrópicas en el crecimiento y desarrollo de las células madre. En las revisiones de la literatura no existen estudios histomorfológicos que muestren la localización y distribución de las R-espondinas en diferentes núcleos hipotalámicos. Por esta razón, el propósito de este estudio fue determinar la localización, características de distribución y densidades en los núcleos hipotalámicos de neuronas que expresan las proteínas Rspo1 y Rspo3. Secciones de cerebro flotantes de ratas macho que no fueron expuestas a ningún tratamiento se tiñeron con el método de inmunoperoxidasa indirecta utilizando los anticuerpos pertinentes. Como resultado de los estudios inmunohistoquímicos, se determinó que las neuronas que expresan la proteína Rspo1 se encontraron en gran número en el núcleo supraóptico (SON), el núcleo supraquiasmático (SCh), el núcleo paraventricular anterior, el núcleo hipotalámico periventricular (PeV), el núcleo hipotalámico anterior área, núcleo preóptico magnocelular (MCPO) y el área hipotalámica lateral (LH) de los núcleos hipotalámicos, mientras que se localizaron en menor número en el núcleo arqueado (ARC). La expresión de la proteína Rspo3 se encontró en neuronas localizadas en los núcleos hipotalámicos SON, núcleo paraventricular (PVN), PeV, ARC, núcleo ventromedial (VMH), LH, núcleo parvicelular anterior y zona inserta (ZI). Además, se encontraron neuronas que sintetizan ambos péptidos en las regiones de la corteza y el hipocampo (H). Las proteínas Rspo1 y 3 se expresan en áreas homeostáticas de energía hipotalámicas, por lo que estas proteínas pueden estar involucradas en la regulación de la ingesta de alimentos.


Subject(s)
Animals , Male , Rats , Thrombospondins/metabolism , Hypothalamus/metabolism , Immunohistochemistry , Rats, Sprague-Dawley
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