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2.
Neurología (Barc., Ed. impr.) ; 39(3): 292-301, Abr. 2024. ilus
Artigo em Inglês | IBECS | ID: ibc-VR-231

RESUMO

Introduction: This paper highlights the relationship of inflammation and oxidative stress as damage mechanisms of Multiple Sclerosis (MS), considered an inflammatory and autoimmune disease. Development: The oxidative stress concept has been defined by an imbalance between oxidants and antioxidants in favor of the oxidants. There is necessary to do physiological functions, like the respiration chain, but in certain conditions, the production of reactive species overpassed the antioxidant systems, which could cause tissue damage. On the other hand, it is well established that inflammation is a complex reaction in the vascularized connective tissue in response to diverse stimuli. However, an unregulated prolonged inflammatory process also can induce tissue damage. Conclusion: Both inflammation and oxidative stress are interrelated since one could promote the other, leading to a toxic feedback system, which contributes to the inflammatory and demyelination process in MS.(AU)


Introducción: Este trabajo destaca la relación de la inflamación y el estrés oxidativo como mecanismos de daño de la esclerosis múltiple, considerada enfermedad inflamatoria y autoinmune. Desarrollo: El concepto de estrés oxidativo se ha definido por un desequilibrio entre oxidantes y antioxidantes a favor de los oxidantes. Es necesario para realizar funciones fisiológicas, como la cadena respiratoria, pero en ciertas condiciones la producción de especies reactivas sobrepasaba los sistemas antioxidantes, lo que podría causar daño tisular. Por otro lado, está establecido que la inflamación es una reacción compleja en el tejido conectivo vascularizado en respuesta a diversos estímulos, pero un proceso inflamatorio prolongado no regulado también puede inducir daño tisular. Conclusión: Tanto la inflamación como el estrés oxidativo están interrelacionados entre sí, ya que uno de ellos podría promover al otro, dando lugar a un sistema de retroalimentación tóxico, que contribuye al desarrollo del proceso inflamatorio y desmielinizante en la esclerosis múltiple.(AU)


Assuntos
Humanos , Masculino , Feminino , Inflamação , Estresse Oxidativo , Neurologia , Doenças do Sistema Nervoso , Esclerose Múltipla
3.
Neurología (Barc., Ed. impr.) ; 39(3): 302-311, Abr. 2024. ilus
Artigo em Espanhol | IBECS | ID: ibc-VR-232

RESUMO

Objetivo: Revisar la evidencia científica disponible sobre la relación entre la periodontitis y las enfermedades neurológicas, en particular la enfermedad cerebrovascular y la demencia. Además, se facilitan una serie de recomendaciones en relación con la prevención y el manejo de la periodontitis y estas enfermedades neurológicas desde las consultas dentales y las unidades de neurología. Desarrollo: Se realizó una búsqueda bibliográfica sin restricción en cuanto al diseño del estudio para identificar aquellos artículos más relevantes sobre la asociación entre periodontitis, enfermedad cerebrovascular y demencia desde un punto de vista epidemiológico, de intervención, así como de mecanismos biológicos involucrados en estas relaciones, y así responder a diferentes preguntas planteadas por los miembros del Grupo de Trabajo SEPA-SEN. Conclusiones: La periodontitis aumenta el riesgo de ictus isquémico y demencia de tipo Alzheimer. Bacteriemias recurrentes con aumento de un estado inflamatorio sistémico de bajo grado parecen ser posibles mecanismos biológicos que explicarían esta asociación. Una evidencia limitada apunta a que diferentes intervenciones de salud oral pueden reducir el riesgo futuro de padecer enfermedad cerebrovascular y demencia.(AU)


Objective: This article reviews the scientific evidence on the relationship between periodontitis and neurological disease, and particularly cerebrovascular disease and dementia. We also issue a series of recommendations regarding the prevention and management of periodontitis and these neurological diseases at dental clinics and neurology units. Development: In response to a series of questions proposed by the SEPA-SEN Working Group, a literature search was performed, with no restrictions on study design, to identify the most relevant articles on the association between periodontitis and cerebrovascular disease and dementia from the perspectives of epidemiology, treatment, and the biological mechanisms involved in these associations. Conclusions: Periodontitis increases the risk of ischaemic stroke and Alzheimer dementia. Recurrent bacterial infections and increased low-grade systemic inflammation seem to be possible biological mechanisms underlying this association. Limited evidence suggests that various oral health interventions can reduce the future risk of cerebrovascular disease and dementia.(AU)


Assuntos
Humanos , Masculino , Feminino , Acidente Vascular Cerebral , Doença de Alzheimer , Demência , Periodontite , Inflamação , Neurologia , Doenças do Sistema Nervoso , Periodonto , Espanha
4.
Int. j. clin. health psychol. (Internet) ; 24(1): [100433], Ene-Mar, 2024. tab, ilus
Artigo em Inglês | IBECS | ID: ibc-230376

RESUMO

Background: The exact causal mechanisms of depression remain unclear due to the complexity of the triggers, which has led to limitations in treating depression using modern drugs. High-intensity interval training (HIIT) is as effective as medication in treating depression without toxic side effects. Typically, HIIT requires less time commitment (i.e., shorter exercise duration) and exhibits pronounced benefits on depressive symptoms than other forms of physical exercise. This review summarizes the risk reduction and clinical effects of HIIT for depression and discusses the underlying mechanisms, providing a theoretical basis for utilizing HIIT in treating depression. Methods: A database search was conducted in PubMed, Embase, Web of Science, and Scopus from inception up to October 2022. The methodological quality of the included literature was evaluated by the physiotherapy evidence database (PEDro) scale criteria. The review focused on evaluating the changes in depression risk or symptoms of HIIT interventions in healthy individuals, patients with depression, and patients with other disorders co-morbid with depression. Consequently, the mechanisms associated with depression related HIIT were summarized. Results: A total of 586 participants (52 % female; mean age: 43.58±8.93 years) from 22 studies were included. Implementing HIIT using different exercise types alleviates depressive symptoms in individuals with depression and in individuals with depression who have exhibited comorbidities and reduced depression scale scores in subjects immediately after acute exercise. In addition, the long-interval HIIT and short-interval HIIT in the treatment of patients with cardiovascular or psychiatric disorders may reduce depressive symptoms via complex exercise-related changes on several levels, including by effecting the following measures: releasing monoamines, reducing neuronal death, inducing neurogenesis, modulating the functional...(AU)


Assuntos
Humanos , Masculino , Feminino , Depressão , Inflamação/reabilitação , Fatores de Crescimento Neural , Sistema Hipotálamo-Hipofisário , Treinamento Intervalado de Alta Intensidade , Tratamento Farmacológico
5.
Allergol. immunopatol ; 52(2): 60-67, mar. 2024. ilus, graf
Artigo em Inglês | IBECS | ID: ibc-231086

RESUMO

Objective: To explore the role of Y-box binding protein 1 (YBX-1) in the lipopolysaccharide (LPS)-stimulated inflammation and oxidative stress of BEAS-2B cell line and clarify the underlying mechanism. Methods: LPS-stimulated BEAS-2B cells were used as a cell model of sepsis-stimulated acute lung injury (ALI). Immunoblot and quantitative polymerase chain reaction assays were used to detect the expression of YBX-1 in LPS-stimulated BEAS-2B cells. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide, TdT-mediated dUTP nick end labeling, and immunoblot assays were conducted to determine the effects of YBX-1 on cell survival. JC-1 staining and adenosine triphosphate production were used to detect the effects of YBX-1 on mitochondrial function. Immunostaining and enzyme-linked immunosorbent serologic assay were performed to examine the effects of YBX-1 on the inflammation and oxidative stress of cells. Immunoblot assay was conducted to confirm the mechanism. Results: YBX-1 was lowly expressed in LPS-stimulated BEAS-2B cells and enhanced the survival of LPS-stimulated lung epithelial cells. In addition, YBX-1 improved mitochondrial function of LPS-stimulated BEAS-2B cells. YBX-1 inhibited the inflammation and oxidative stress of LPS-stimulated BEAS-2B cells. Mechanically, YBX-1 inhibited mitogen-activated protein kinase (MAPK) axis, thereby alleviating sepsis-stimulated ALI. Conclusion: YBX-1 alleviated inflammation and oxidative stress of LPS-stimulated BEAS-2B cells via MAPK axis. (AU)


Assuntos
Humanos , Proteína 1 de Ligação a Y-Box , Inflamação , Lipopolissacarídeos , Lesão Pulmonar Aguda , Sepse , Sobrevivência Celular , Células Epiteliais Alveolares
9.
Nefrología (Madrid) ; 44(1): 10-22, ene.- feb. 2024. tab, ilus
Artigo em Inglês | IBECS | ID: ibc-229417

RESUMO

Receptor interacting protein kinase 3 (RIPK3) is an intracellular kinase at the crossroads of cell death and inflammation. RIPK3 contains a RIP homotypic interaction motif (RHIM) domain which allows interactions with other RHIM-containing proteins and a kinase domain that allows phosphorylation of target proteins. RIPK3 may be activated through interaction with RHIM-containing proteins such as RIPK1, TRIF and DAI (ZBP1, DLM-1) or through RHIM-independent mechanisms in an alkaline intracellular pH. RIPK3 mediates necroptosis and promotes inflammation, independently of necroptosis, through either activation of NFκB or the inflammasome. There is in vivo preclinical evidence of the contribution of RIPK3 to both acute kidney injury (AKI) and chronic kidney disease (CKD) and to the AKI-to-CKD transition derived from RIPK3 deficient mice or the use of small molecule RIPK3 inhibitors. In these studies, RIPK3 targeting decreased inflammation but kidney injury improved only in some contexts. Clinical translation of these findings has been delayed by the potential of some small molecule inhibitors of RIPK3 kinase activity to trigger apoptotic cell death by inducing conformational changes of the protein. A better understanding of the conformational changes in RIPK3 that trigger apoptosis, dual RIPK3/RIPK1 inhibitors or repurposing of multiple kinase inhibitors such as dabrafenib may facilitate clinical development of the RIPK3 inhibition concept for diverse inflammatory diseases, including kidney diseases (AU)


La proteína quinasa 3 que interactúa con el receptor (RIPK3) es una quinasa intracelular que se encuentra a medio camino entre la muerte celular y la inflamación. La RIPK3 contiene un dominio motivo de interacción homotípica de RIP (RHIM), que permite las interacciones con otras proteínas que contienen RHIM, y un dominio de quinasa que permite la fosforilación de las proteínas diana. La RIPK3 puede ser activada a través de la interacción con las proteínas que contienen RHIM tales como RIPK1, TRIF y DAI (ZBP1, DLM-1), o a través de mecanismos independientes de RHIM en un pH intracelular alcalino. La RIPK3 media en la necroptosis y promueve la inflamación, independientemente de la necroptosis, bien a través de la activación de NFκB, o del inflamasoma. Existe evidencia preclínica in vivo de la contribución de RIPK3 a la insuficiencia renal aguda (IRA) y la enfermedad renal crónica (ERC), así como a la transición IRA-ERC derivada de ratones con deficiencia de RIPK3 o del uso de pequeñas moléculas inhibidoras de RIPK3. En dichos estudios, el tener a RIPK3 como objetivo redujo la inflamación, pero la nefropatía mejoró solo en algunos contextos. La traducción clínica de estos hallazgos se ha demorado debido al potencial de ciertas pequeñas moléculas inhibidoras de la actividad de la quinasa RIPK3 para activar la muerte celular induciendo cambios conformacionales de la proteína. Comprender mejor los cambios conformacionales de RIPK3 activadores de la apoptosis, los inhibidores duales RIPK3/RIPK1 o la reconversión de múltiples inhibidores de la quinasa tales como dabrafenib podría facilitar el desarrollo clínico del concepto de la inhibición de RIPK3 para diversas enfermedades inflamatorias, incluyendo las enfermedades renales (AU)


Assuntos
Humanos , Insuficiência Renal/metabolismo , Inflamação , Concentração Osmolar , Proteína Quinase 3 Ativada por Mitógeno , Doença Aguda
10.
Radiología (Madr., Ed. impr.) ; 66(1): 32-46, Ene-Feb, 2024. ilus, tab
Artigo em Espanhol | IBECS | ID: ibc-229644

RESUMO

Objetivo: Describir los hallazgos en resonancia magnética (RM) de las principales enfermedades inflamatorias e inmunomediadas que afectan al troncoencéfalo. Conclusión: El diagnóstico diferencial de las lesiones inflamatorias localizadas en el troncoencéfalo es complicado debido al amplio espectro de enfermedades autoinmunes, infecciosas y síndromes paraneoplásicos que pueden causarlas. Conocer estas entidades, sus características clínicas y sus manifestaciones en RM, sobre todo en cuanto a número, morfología, extensión y apariencia en las diferentes secuencias, es útil a la hora de orientar el diagnóstico radiológico.(AU)


Objective: To describe the magnetic resonance imaging (MRI) findings for the most common inflammatory and immune-mediated diseases that involve the brainstem. Conclusion: Inflammatory lesions involving the brainstem are associated with a wide range of autoimmune, infectious, and paraneoplastic syndromes, making the differential diagnosis complex. Being familiar with these entities, their clinical characteristics, and their manifestations on MRI, particularly the number of lesions, their shape and extension, and their appearance in different sequences, is useful for orienting the radiological diagnosis.(AU)


Assuntos
Humanos , Masculino , Feminino , Diagnóstico Diferencial , Espectroscopia de Ressonância Magnética , Tegmento Mesencefálico , Mesencéfalo/diagnóstico por imagem , Inflamação/diagnóstico por imagem , Tronco Encefálico , Radiologia/métodos , Diagnóstico por Imagem , Doenças Autoimunes
11.
J. physiol. biochem ; 80(1): 11-26, Feb. 2024.
Artigo em Inglês | IBECS | ID: ibc-229937

RESUMO

Fatty liver index (FLI) was developed as a simple and accurate marker of hepatic steatosis. FLI is derived from an algorithm based on body mass index, waist circumference, and levels of triglycerides and gamma-glutamyltransferase, and it is widely used in clinical and epidemiological studies as a screening tool for discriminating between healthy and nonalcoholic fatty liver disease (NAFLD) subjects. However, a systematic review of the literature regarding FLI revealed that this index has more extensive relationships with biochemical and physiological parameters. FLI is associated with key parameters of lipid, protein and carbohydrate metabolism, hormones, vitamins and markers of inflammation, or oxidative stress. FLI can be a predictor or risk factor for a number of metabolic and nonmetabolic diseases and mortality. FLI is also used as an indicator for determining the effects of health-related prevention interventions, medications, and toxic substances on humans. Although in most cases, the exact mechanisms underlying these associations have not been fully elucidated, they are most often assumed to be mediated by insulin resistance, inflammation, and oxidative stress. Thus, FLI may be a promising marker of metabolic health due to its multiple associations with parameters of physiological and pathological processes. In this context, the present review summarizes the data from currently available literature on the associations between FLI and biochemical variables and physiological functions. We believe that this review will be of interest to researchers working in this area and can provide new perspectives and directions for future studies on FLI. (AU)


Assuntos
Fígado Gorduroso , Fatores de Risco , Resistência à Insulina , Estresse Oxidativo , Inflamação
12.
J. physiol. biochem ; 80(1): 161-173, Feb. 2024. graf
Artigo em Inglês | IBECS | ID: ibc-229948

RESUMO

Resistance training (RT) can increase the heat shock response (HSR) in the elderly. As middle-aged subjects already suffer physiological declines related to aging, it is hypothesized that RT may increase the HSR in these people. To assess the effects of resistance training on heat shock response, intra and extracellular HSP70, oxidative stress, inflammation, body composition, and metabolism in middle-aged subjects. Sixteen volunteers (40 – 59 years) were allocated to two groups: the trained group (n = 7), which performed 12 weeks of RT; and the physically inactive—control group (n = 9), which did not perform any type of exercise. The RT program consisted of 9 whole-body exercises (using standard gym equipment) and functional exercises, carried out 3 times/week. Before and after the intervention, body composition, muscle mass, strength, functional capacity, and blood sample measurements (lipid profile, glucose, insulin, oxidative damage, TNF-α, the HSR, HSP70 expression in leukocytes, and HSP72 in plasma) were performed. The HSR analysis demonstrated that this response is maintained at normal levels in middle-aged people and that RT did not cause any improvement. Also, RT increases muscle mass, strength, and functional capacity. Despite no additional changes of RT on the antioxidant defenses (catalase, glutathione peroxidase, and reductase) or inflammation, lipid peroxidation was diminished by RT (group x time interaction, p = 0.009), indicating that other antioxidant defenses may be improved after RT. HSR is preserved in middle-aged subjects without metabolic complications. In addition, RT reduces lipid peroxidation and can retard muscle mass and strength loss related to the aging process. (AU)


Assuntos
Humanos , Pessoa de Meia-Idade , Resposta ao Choque Térmico , Treinamento de Força , Proteínas de Choque Térmico HSP70 , Estresse Oxidativo , Inflamação , Metabolismo
13.
J. physiol. biochem ; 80(1): 175-188, Feb. 2024. ilus, graf
Artigo em Inglês | IBECS | ID: ibc-229949

RESUMO

Lipotoxicity-induced pancreatic β cell damage is a strong predictor of type 2 diabetes mellitus (T2DM). Our previous work showed that Caveolin-1 (Cav-1) depletion decreased β-cell apoptosis and improved β-cell viability. Further microarray analysis indicated significant changes in the expression of genes related to fatty acid metabolism and inflammation. The objective of this study was to explore the role of Cav-1 in intracellular lipid accumulation and inflammation in β cells under lipotoxic conditions. Here, we established a β-cell-specific Cav-1 knockout (β-Cav-1 KO) mouse model and a CAV-1 depleted β cell line (NIT-1). We found that Cav-1 silencing significantly reduced palmitate (PA)-induced intracellular triglyceride (TG) accumulation and decreased proinflammatory factor expression in both the mouse and cell models. Further mechanistic investigation revealed that amelioration of lipid metabolism was achieved through the downregulation of lipogenic markers (SREBP-1c, FAS and ACC) and upregulation of a fatty acid oxidation marker (CPT-1). Meanwhile, decrease of inflammatory cytokines (IL-6, TNF-α, and IL-1β) secretion was found with the involvement of the IKKβ/NF-κB signaling pathways. Our findings suggest that Cav-1 is of considerable importance in regulating lipotoxicity-induced β-cell intracellular lipid accumulation and inflammation. (AU)


Assuntos
Caveolina 1/deficiência , Células Secretoras de Insulina , Inflamação , Palmitatos
14.
Med. clín (Ed. impr.) ; 162(4): 182-189, Feb. 2024. ilus, graf
Artigo em Espanhol | IBECS | ID: ibc-230575

RESUMO

La hidradenitis supurativa (HS) es una enfermedad inflamatoria crónica y recurrente derivada de la unidad pilosebácea, que afecta aproximadamente al 1% de la población general. Se caracteriza clínicamente por nódulos inflamatorios, abscesos y túneles en las áreas intertriginosas del cuerpo, especialmente en las regiones axilar, inguinal y anogenital. La etiopatogenia de la HS no está totalmente aclarada, aunque se considera que es multifactorial, y resultado de una compleja interacción entre factores genéticos, hormonales, ambientales e inmunológicos. En este sentido, determinadas citocinas proinflamatorias como el factor de necrosis tumoral-alfa (TNF-α), la interleucina (IL)-1β y la IL-17, entre otras, parecen desempeñar un papel fundamental en la patogénesis de la enfermedad. Actualmente, la HS es considerada una enfermedad inflamatoria sistémica asociada con numerosas comorbilidades, incluyendo enfermedades cardiovasculares, inmunomediadas y trastornos endocrino-metabolicos. El tratamiento de la HS debe realizarse con un enfoque individualizado y orientado al paciente, considerando modalidades de tratamiento médico y quirúrgico.(AU)


Hidradenitis suppurativa (HS) is a chronic and debilitating inflammatory disease derived from the pilosebaceous unit, that affects approximately 1% of the general population. Clinically, it is characterized by inflammatory nodules, abscesses, and tunnels in the intertriginous areas of the body, especially in the axillary, inguinal, and anogenital regions. The etiopathogenesis of HS is not completely understood, although it is considered to be multifactorial, and the result of a complex interaction between genetic, hormonal, environmental, and immunological factors. In this sense, several proinflammatory cytokines, such as tumor necrosis factor-alpha (TNF-α), interleukin (IL)-L-1β, and IL-17, among others, appear to play a crucial role in the pathogenesis of the disease. Currently, HS is recognized as a systemic disease associated with numerous comorbidities, including cardiovascular, immune-mediated, and endocrine-metabolic diseases. The treatment of HS must be carried out with an individualized and patient-oriented approach, considering medical and surgical treatment modalities.(AU)


Assuntos
Humanos , Masculino , Comorbidade , Inflamação , Hidradenite Supurativa/diagnóstico por imagem , Hidradenite Supurativa/etiologia , Hidradenite Supurativa/epidemiologia , Medicina Clínica , Hidradenite Supurativa/tratamento farmacológico , Microbiota
15.
J. physiol. biochem ; 80(1): 11-26, Feb. 2024.
Artigo em Inglês | IBECS | ID: ibc-EMG-562

RESUMO

Fatty liver index (FLI) was developed as a simple and accurate marker of hepatic steatosis. FLI is derived from an algorithm based on body mass index, waist circumference, and levels of triglycerides and gamma-glutamyltransferase, and it is widely used in clinical and epidemiological studies as a screening tool for discriminating between healthy and nonalcoholic fatty liver disease (NAFLD) subjects. However, a systematic review of the literature regarding FLI revealed that this index has more extensive relationships with biochemical and physiological parameters. FLI is associated with key parameters of lipid, protein and carbohydrate metabolism, hormones, vitamins and markers of inflammation, or oxidative stress. FLI can be a predictor or risk factor for a number of metabolic and nonmetabolic diseases and mortality. FLI is also used as an indicator for determining the effects of health-related prevention interventions, medications, and toxic substances on humans. Although in most cases, the exact mechanisms underlying these associations have not been fully elucidated, they are most often assumed to be mediated by insulin resistance, inflammation, and oxidative stress. Thus, FLI may be a promising marker of metabolic health due to its multiple associations with parameters of physiological and pathological processes. In this context, the present review summarizes the data from currently available literature on the associations between FLI and biochemical variables and physiological functions. We believe that this review will be of interest to researchers working in this area and can provide new perspectives and directions for future studies on FLI. (AU)


Assuntos
Fígado Gorduroso , Fatores de Risco , Resistência à Insulina , Estresse Oxidativo , Inflamação
16.
J. physiol. biochem ; 80(1): 161-173, Feb. 2024. graf
Artigo em Inglês | IBECS | ID: ibc-EMG-574

RESUMO

Resistance training (RT) can increase the heat shock response (HSR) in the elderly. As middle-aged subjects already suffer physiological declines related to aging, it is hypothesized that RT may increase the HSR in these people. To assess the effects of resistance training on heat shock response, intra and extracellular HSP70, oxidative stress, inflammation, body composition, and metabolism in middle-aged subjects. Sixteen volunteers (40 – 59 years) were allocated to two groups: the trained group (n = 7), which performed 12 weeks of RT; and the physically inactive—control group (n = 9), which did not perform any type of exercise. The RT program consisted of 9 whole-body exercises (using standard gym equipment) and functional exercises, carried out 3 times/week. Before and after the intervention, body composition, muscle mass, strength, functional capacity, and blood sample measurements (lipid profile, glucose, insulin, oxidative damage, TNF-α, the HSR, HSP70 expression in leukocytes, and HSP72 in plasma) were performed. The HSR analysis demonstrated that this response is maintained at normal levels in middle-aged people and that RT did not cause any improvement. Also, RT increases muscle mass, strength, and functional capacity. Despite no additional changes of RT on the antioxidant defenses (catalase, glutathione peroxidase, and reductase) or inflammation, lipid peroxidation was diminished by RT (group x time interaction, p = 0.009), indicating that other antioxidant defenses may be improved after RT. HSR is preserved in middle-aged subjects without metabolic complications. In addition, RT reduces lipid peroxidation and can retard muscle mass and strength loss related to the aging process. (AU)


Assuntos
Humanos , Pessoa de Meia-Idade , Resposta ao Choque Térmico , Treinamento de Força , Proteínas de Choque Térmico HSP70 , Estresse Oxidativo , Inflamação , Metabolismo
17.
J. physiol. biochem ; 80(1): 175-188, Feb. 2024. ilus, graf
Artigo em Inglês | IBECS | ID: ibc-EMG-575

RESUMO

Lipotoxicity-induced pancreatic β cell damage is a strong predictor of type 2 diabetes mellitus (T2DM). Our previous work showed that Caveolin-1 (Cav-1) depletion decreased β-cell apoptosis and improved β-cell viability. Further microarray analysis indicated significant changes in the expression of genes related to fatty acid metabolism and inflammation. The objective of this study was to explore the role of Cav-1 in intracellular lipid accumulation and inflammation in β cells under lipotoxic conditions. Here, we established a β-cell-specific Cav-1 knockout (β-Cav-1 KO) mouse model and a CAV-1 depleted β cell line (NIT-1). We found that Cav-1 silencing significantly reduced palmitate (PA)-induced intracellular triglyceride (TG) accumulation and decreased proinflammatory factor expression in both the mouse and cell models. Further mechanistic investigation revealed that amelioration of lipid metabolism was achieved through the downregulation of lipogenic markers (SREBP-1c, FAS and ACC) and upregulation of a fatty acid oxidation marker (CPT-1). Meanwhile, decrease of inflammatory cytokines (IL-6, TNF-α, and IL-1β) secretion was found with the involvement of the IKKβ/NF-κB signaling pathways. Our findings suggest that Cav-1 is of considerable importance in regulating lipotoxicity-induced β-cell intracellular lipid accumulation and inflammation. (AU)


Assuntos
Caveolina 1/deficiência , Células Secretoras de Insulina , Inflamação , Palmitatos
18.
Arch. esp. urol. (Ed. impr.) ; 77(1): 67-71, 28 jan. 2024. tab
Artigo em Inglês | IBECS | ID: ibc-230500

RESUMO

Background: Acute kidney injury (AKI) is common in patients with sepsis and may result in death. Systemic immune inflammation index (SII) is associated with kidney injury, but its predictive value for AKI in patients with sepsis remains unclear. Objective: This study aimed to explore the predictive value of SII in sepsis patients with AKI. Methods: From January 2020 to December 2022, 221 patients with sepsis treated in our hospital were retrospectively collected. The patients were divided into AKI group (n = 61) and control group (n = 160). Clinical characteristics and SII level were compared between the two groups, and the predictive value of SII for the occurrence of AKI was analysed. Results: The SII level (724.72 ± 235.50 vs. 522.38 ± 205.62, p < 0.001), the serum procalcitonin level (8.13 ± 15.52 vs. 4.52 ± 10.34 µg/L, p < 0.001), and the acute physiology and chronic health evaluation II score (14.26 ± 2.90 vs. 11.62 ± 2.26, p < 0.001) significantly increased in the AKI group compared with the control group, whereas the albumin level significantly decreased (30.60 ± 5.41 vs. 32.49 ± 5.31 g/L, p = 0.019). The receiver operating characteristic curve showed that SII was valuable in predicting AKI in patients with sepsis, with an area under the curve of 0.733 (95% confidence interval: 0.657–0.810, p < 0.001). The continuous renal replacement therapy intervention rate (88.52% vs. 0.00%, p < 0.001), the intervention rate of vasoactive drugs (34.43% vs. 3.75%, p < 0.001), and the hospital mortality rate (16.39% vs. 2.50%, p < 0.001) significantly increased in the AKI group compared with the control group. Conclusions: AKI was associated with poor prognosis in patients with sepsis. SII, procalcitonin and acute physiology and chronic health evaluation II (APACHE II) score were valuable in predicting the occurrence of AKI. SII may serve as a new marker in patients with sepsis (AU)


Assuntos
Humanos , Masculino , Feminino , Adulto , Pessoa de Meia-Idade , Idoso , Injúria Renal Aguda/sangue , Injúria Renal Aguda/patologia , Inflamação , Sepse , Valor Preditivo dos Testes , Estudos Retrospectivos
19.
Allergol. immunopatol ; 52(1): 1-8, 01 jan. 2024. ilus, graf
Artigo em Inglês | IBECS | ID: ibc-229170

RESUMO

Background: Resveratrol has been found to have anti-inflammatory and anti-allergic proper-ties. The effects of resveratrol on thymic stromal lymphopoietin (TSLP)-mediated atopic march remain unclear. Purpose: To explore the potential role of resveratrol in TSLP-mediated atopic march.Methods: The atopic march mouse model was established by topical application of MC903 (a vitamin D3 analog). Following the treatment with resveratrol, airway resistance in mice was discovered by pulmonary function apparatus, and the number of total cells, neutrophils, and eosinophils in bronchoalveolar lavage fluid was counted. The histopathological features of pul-monary and ear skin tissues, inflammation, and cell infiltration were determined by hematoxy-lin and eosin staining. The messenger RNA (mRNA) levels of TSLP, immunoglobulin E, interleukin (IL)-4, IL-5, and IL-13 were measured by real-time quantitative polymerase chain reaction. The protein expression of nuclear factor kappa B (NF-κB)/nuclear factor erythroid 2-related factor 2 (Nrf2) signaling-associated molecules (p-p65, p65, p-I kappa B kinase alpha (IκBα), IκBα, Nrf2, and TSLP) in lung and ear skin tissues were assessed by Western blot analysis.Results: Resveratrol attenuated airway resistance and infiltration of total cells, eosinophils, and neutrophils in both lung and ear skin tissues. Resveratrol ameliorates serum inflammatory markers in allergic mice. Moreover, the phosphorylation levels of NF-κB pathway-related pro-teins were significantly reduced by administration of resveratrol in allergic lung and ear skin tissues. Similarly, the protein expression of TSLP in both lung and ear skin tissues was reduced by resveratrol, and Nrf2, a protector molecule, was increased with resveratrol treatment (AU)


Assuntos
Animais , Camundongos , Fator 2 Relacionado a NF-E2/genética , Hipersensibilidade Imediata/tratamento farmacológico , Resveratrol/administração & dosagem , Modelos Animais de Doenças , Transdução de Sinais , Inflamação
20.
Med. oral patol. oral cir. bucal (Internet) ; 29(1): e9-e17, Ene. 2024. tab, ilus
Artigo em Inglês | IBECS | ID: ibc-229183

RESUMO

Background: Chitosan is a cheap, accessible, nontoxic, biocompatible, and biodegradable compound. Also, thispolysaccharide possesses antibacterial and anti-inflammatory properties. Consequently, a wide range of chitosanapplications in the dentistry field has been explored. This work aimed to conduct a systematic review to addressthe clinical efficacy of chitosan for the treatment of oral mucositis.Material and Methods: The design of the included studies were observational studies, randomized clinical trials(RCT), and non-randomized clinical trials (non-RCT), whereas, a series of cases, in vivo, and in vitro studies wereexcluded. The search was performed in PubMed, Web of Science, Scopus, Dentistry and Oral Sciences Source,and ClinicalTrials. Gray literature was searched at Google Scholar. Relevant data from all included studies wererecorded. The risk of bias (using RoB 2) and the quality (using Grading of Recommendations Assessment, Devel-opment, and Evaluation, GRADE) assessments were carried out.Results: From the 8413 records screened, 5 clinical trials fully met the eligibility criteria, which comprised a totalof 192 participants suffering oral lesions and pain related to oral mucositis. 100% of the included studies exhibiteda high risk of bias. The quality of the studies was between low and very low.Conclusions: The results of the included studies suggest that chitosan can diminish pain and improve the healingof ulcers in oral mucositis. However, there is no conclusive evidence of chitosan as a superior treatment for oralmucositis compared with other current therapies.(AU)


Assuntos
Humanos , Masculino , Feminino , Cicatrização , Quitosana , Inflamação/tratamento farmacológico , Mucosa Bucal , Quitosana/uso terapêutico , Dor/tratamento farmacológico , Doenças da Boca , Saúde Bucal , Odontologia , Medicina Bucal
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