Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 13 de 13
Filtrar
Más filtros











Base de datos
Intervalo de año de publicación
1.
J Therm Biol ; 119: 103782, 2024 Jan.
Artículo en Inglés | MEDLINE | ID: mdl-38176292

RESUMEN

Enhanced vascular permeability at the site of injury is a prominent feature in acute inflammatory pain models, commonly assessed through the Evans Blue test. However, this invasive test requires euthanasia, thereby precluding further investigations on the same animal. Due to these limitations, the integration of non-invasive tools such as IRT has been sought. Here, we aimed to evaluate the use of thermography in a common orofacial pain model that employs formalin as a chemical irritant to induce local orofacial inflammation. Male Hannover rats (290-300 g, N = 43) were used. In the first approach, radiometric images were taken before and after formalin administration, assessing temperature changes and extravasated Evans Blue. The second approach included capturing pre- and post-formalin test radiometric images, followed by cytokine measurements in excised vibrissae tissue. Rats were anesthetized for vibrissae tissue collection, allowing correlations between thermographic patterns, nocifensive behavior duration, and cytokine levels in this area. Our findings revealed a positive correlation between local temperature, measured via thermography, and vascular permeability in the contralateral (r2 = 0.3483) and ipsilateral (r2 = 0.4502) side, measured using spectrophotometry. The obtained data supports the notion that thermography-based temperature assessment can effectively evaluate vascular permeability in the orofacial region.


Asunto(s)
Formaldehído , Termografía , Ratas , Masculino , Animales , Formaldehído/efectos adversos , Termografía/métodos , Permeabilidad Capilar , Azul de Evans/efectos adversos , Dolor Facial/inducido químicamente , Citocinas
2.
Arch Oral Biol ; 152: 105734, 2023 Aug.
Artículo en Inglés | MEDLINE | ID: mdl-37244090

RESUMEN

Orofacial pain has significant psychological and physiological effects. Citral (3,7-dimethyl-2,6-octadienal) is the main component of Cymbopogon citratus (DC) Stapf, an herb with analgesic properties. Although citral has been considered a potent analgesic, its putative effects on orofacial pain are still unknown. OBJECTIVE: The objective of this study is to test the hypothesis that citral modulates orofacial pain using two experimental models: formalin-induced hyperalgesia in the vibrissae area and during persistent temporomandibular hypernociception using Complete Freund's Adjuvant - CFA test. METHODS: For the formalin test, citral (100 and 300 mg/kg, oral gavage) or its vehicle (Tween 80, 1 %) were given 1 h before the formalin injection subcutaneously (sc) into the vibrissae area. For the CFA model, we analyzed the prophylactic (100 mg/kg of citral by oral gavage, 1 h before CFA injection) and the chronic therapeutic (citral treatment 1-hour post-CFA injection and daily post-CFA injection) effect of citral or its vehicle in animals treated with CFA for 8 days. RESULTS: Citral caused a decrease in formalin-induced local inflammation and the time spent performing nociceptive behavior in a dose-dependent fashion. Similarly, prophylactic and therapeutic citral treatment decreased the CFA-induced persistent mechanical hypernociception in the temporomandibular area. CONCLUSION: Our data strengthen the notion that citral plays a powerful antinociceptive role by decreasing orofacial hypernociception in formalin and CFA models.


Asunto(s)
Dolor Facial , Hiperalgesia , Ratas , Animales , Hiperalgesia/tratamiento farmacológico , Dolor Facial/tratamiento farmacológico , Dolor Facial/etiología , Inflamación/tratamiento farmacológico , Inflamación/inducido químicamente , Analgésicos/farmacología , Formaldehído
3.
Brain Behav Immun Health ; 30: 100623, 2023 Jul.
Artículo en Inglés | MEDLINE | ID: mdl-37096172

RESUMEN

L-3,4-dihydroxyphenylalanine (L-DOPA)-induced dyskinesia is a side effect of Parkinson's disease treatment and it is characterized by atypical involuntary movements. A link between neuroinflammation and L-DOPA-induced dyskinesia has been documented. Hydrogen gas (H2) has neuroprotective effects in Parkinson's disease models and has a major anti-inflammatory effect. Our objective is to test the hypothesis that H2 inhalation reduces L-DOPA-induced dyskinesia. 15 days after 6-hydroxydopamine lesions of dopaminergic neurons were made (microinjection into the medial forebrain bundle), chronic L-DOPA treatment (15 days) was performed. Rats were exposed to H2 (2% gas mixture, 1 h) or air (controls) before L-DOPA injection. Abnormal involuntary movements and locomotor activity were conducted. Striatal microglia and astrocyte was analyzed and striatal and plasma samples for cytokines evaluation were collected after the abnormal involuntary movements analysis. H2 inhalation attenuated L-DOPA-induced dyskinesia. The gas therapy did not impair the improvement of locomotor activity achieved by L-DOPA treatment. H2 inhalation reduced activated microglia in the lesioned striatum, which is consistent with the observed reduced pro-inflammatory cytokines levels. Display of abnormal involuntary movements was positively correlated with plasma IL-1ß and striatal TNF-α levels and negatively correlated with striatal IL-10 levels. Prophylactic H2 inhalation decreases abnormal involuntary movements in a preclinical L-DOPA-induced dyskinesia model. The H2 antidyskinetic effect was associated with decreased striatal and peripheral inflammation. This finding has a translational importance to L-DOPA-treated parkinsonian patients' well-being.

4.
Eur J Pharmacol ; 889: 173629, 2020 Dec 15.
Artículo en Inglés | MEDLINE | ID: mdl-33022271

RESUMEN

The absence of a specific treatment for SARS-CoV-2 infection led to an intense global effort in order to find new therapeutic interventions and improve patient outcomes. One important feature of COVID-19 pathophysiology is the activation of immune cells, with consequent massive production and release of inflammatory mediators that may cause impairment of several organ functions, including the brain. In addition to its classical role as a neurotransmitter, serotonin (5-hydroxytryptamine, 5-HT) has immunomodulatory properties, downregulating the inflammatory response by central and peripheral mechanisms. In this review, we describe the roles of 5-HT in the regulation of systemic inflammation and the potential benefits of the use of specific serotonin reuptake inhibitors as a coadjutant therapy to attenuate neurological complications of COVID-19.


Asunto(s)
Tratamiento Farmacológico de COVID-19 , Inflamación/tratamiento farmacológico , Enfermedades del Sistema Nervioso/tratamiento farmacológico , Fármacos Neuroprotectores/uso terapéutico , Inhibidores Selectivos de la Recaptación de Serotonina/uso terapéutico , Animales , COVID-19/complicaciones , Humanos , Inflamación/complicaciones , Enfermedades del Sistema Nervioso/complicaciones , Fármacos Neuroprotectores/farmacología , Pandemias , SARS-CoV-2 , Inhibidores Selectivos de la Recaptación de Serotonina/farmacología
5.
J Physiol ; 598(20): 4663-4680, 2020 10.
Artículo en Inglés | MEDLINE | ID: mdl-32749717

RESUMEN

KEY POINTS: The mechanisms involved in hypothermia and fever during systemic inflammation (SI) remain largely unknown. Our data support the contention that brain-mediated mechanisms are different in hypertension during SI. Considering that, clinically, it is not easy to assess all mechanisms involved in cardiovascular and thermoregulatory control during SI, the present study sheds light on these integrated mechanisms that may be triggered simultaneously in septic hypertensive patients. The result obtained demonstrate that, in lipopolysaccharide-induced SI, an increased hypothermia is observed in neurogenic hypertension, which is caused by reduced hypothalamic prostaglandin E2 production and increased heat loss in conscious rats. Therefore, the results of the present study provide useful insight for clinical trials evaluating the thermoregulatory outcomes of septic patients with hypertension. ABSTRACT: Hypertension is a prevalent disease characterized by autonomic-induced elevated and sustained blood pressure levels and abnormal body core temperature (Tb) regulation. The present study aimed to determine the brain-mediated mechanisms involved in the thermoregulatory changes observed during lipopolysaccharide (LPS)-induced systemic inflammation (SI; at a septic-like model) in spontaneously hypertensive rats (SHR). We combined Tb and skin temperature (Tsk) analysis, assessment of prostaglandin (PG) E2 levels (the proximal mediator of fever) in the anteroventral region of the hypothalamus (AVPO; an important site for Tb control), oxygen consumption analysis, cardiovascular recordings, assays of inflammatory markers, and evaluation of oxidative stress in the plasma and brain of male Wistar rats and SHR that had received LPS (1.5 mg kg-1 ) or saline. LPS induced hypothermia followed by fever in Wistar rats, whereas, in SHR, a maintained hypothermia without fever were observed. These thermoregulatory responses were associated with an increased heat loss in SHR compared to Wistar rats. We measured LPS-induced increased PGE2 levels in the AVPO in Wistar rats, but not in SHR. The LPS-induced drop in blood pressure was higher in SHR than in Wistar rats. Furthermore, LPS-induced plasma and brain [regions involved in autonomic control: nucleus tractus solitarius (NTS) and rostral ventrolateral medulla (RVLM)] cytokine surges were blunted, whereas oxidative stress was higher in SHR. LPS-induced SI leads to blunted cytokine surges both systemically (plasma) and centrally (NTS and RVLM) and reduced hypothalamic PGE2 production, which are all associated with increased hypothermia mediated by increased heat loss, but not by heat production, in SHR.


Asunto(s)
Hipertensión , Hipotermia Inducida , Animales , Regulación de la Temperatura Corporal , Dinoprostona , Humanos , Hipotálamo , Lipopolisacáridos/toxicidad , Masculino , Ratas , Ratas Wistar
6.
Brain Res ; 1739: 146857, 2020 07 15.
Artículo en Inglés | MEDLINE | ID: mdl-32348775

RESUMEN

The central nervous system (CNS) is one of the first physiological systems to be affected in sepsis. During the exacerbated systemic inflammatory response at the early stage of sepsis, circulatory inflammatory mediators are able to reach the CNS leading to neuroinflammation and, consequently, long-term impairment in learning and memory formation is observed. The acute treatment with molecular hydrogen (H2) exerts important antioxidative, antiapoptotic, and anti-inflammatory effects in sepsis, but little is known about the mechanism itself and the efficacy of chronic H2 inhalation in sepsis treatment. Thus, we tested two hypotheses. We first hypothesized that chronic H2 inhalation is also an effective therapy to treat memory impairment induced by sepsis. The second hypothesis is that H2 treatment decreases sepsis-induced neuroinflammation in the hippocampus and prefrontal cortex, important areas related to short and long-term memory processing. Our results indicate that (1) chronic exposure of hydrogen gas is a simple, safe and promising therapeutic strategy to prevent memory loss in patients with sepsis and (2) acute H2 inhalation decreases neuroinflammation in memory-related areas and increases total nuclear factor E2-related factor 2 (Nrf2), a transcription factorthat regulates a vast group of antioxidant and inflammatory agents expression in these areas of septic animals.


Asunto(s)
Hidrógeno/farmacología , Trastornos de la Memoria/terapia , Sepsis/tratamiento farmacológico , Administración por Inhalación , Animales , Antioxidantes/farmacología , Apoptosis/efectos de los fármacos , Encéfalo/efectos de los fármacos , Modelos Animales de Enfermedad , Hipocampo/efectos de los fármacos , Hidrógeno/metabolismo , Inflamación/tratamiento farmacológico , Mediadores de Inflamación/metabolismo , Masculino , Trastornos de la Memoria/metabolismo , Memoria a Largo Plazo/efectos de los fármacos , Memoria a Corto Plazo/efectos de los fármacos , Factor 2 Relacionado con NF-E2/metabolismo , Estrés Oxidativo/efectos de los fármacos , Corteza Prefrontal/efectos de los fármacos , Ratas , Ratas Wistar
7.
Acta Physiol (Oxf) ; 228(3): e13373, 2020 03.
Artículo en Inglés | MEDLINE | ID: mdl-31483934

RESUMEN

AIM: Whereas some patients have important changes in body core temperature (Tb) during systemic inflammation, others maintain a normal Tb, which is intrinsically associated to immune paralysis. One classical model to study immune paralysis is the use of repeated administration of lipopolysaccharide (LPS), the so-called endotoxin tolerance. However, the neuroimmune mechanisms of endotoxin tolerance remain poorly understood. Hydrogen sulphide (H2 S) is a gaseous neuromodulator produced in the brain by the enzyme cystathionine ß-synthase (CBS). The present study assessed whether endotoxin tolerance is modulated by hypothalamic H2 S. METHODS: Rats with central cannulas (drug microinjection) and intraperitoneal datalogger (temperature record) received a low-dose of lipopolysaccharide (LPS; 100 µg kg-1 ) daily for four consecutive days. Hypothalamic CBS expression and H2 S production rate were assessed, together with febrigenic signalling. Tolerant rats received an inhibitor of H2 S synthesis (AOA, 100 pmol 1 µL-1 icv) or its vehicle in the last day. RESULTS: Antero-ventral preoptic area of the hypothalamus (AVPO) H2 S production rate and CBS expression were increased in endotoxin-tolerant rats. Additionally, hypothalamic H2 S inhibition reversed endotoxin tolerance reestablishing fever, AVPO and plasma PGE2 levels without altering the absent plasma cytokines surges. CONCLUSION: Endotoxin tolerance is not simply a reflection of peripheral reduced cytokines release but actually results from a complex set of mechanisms acting at multiple levels. Hypothalamic H2 S production modulates most of these mechanisms.


Asunto(s)
Dinoprostona/biosíntesis , Endotoxinas/farmacología , Sulfuro de Hidrógeno/metabolismo , Hipotálamo/efectos de los fármacos , Hipotálamo/metabolismo , Animales , Cistationina betasintasa/genética , Cistationina betasintasa/metabolismo , Citocinas/metabolismo , Dinoprostona/antagonistas & inhibidores , Dinoprostona/metabolismo , Modelos Animales de Enfermedad , Tolerancia a Medicamentos , Fiebre/tratamiento farmacológico , Fiebre/metabolismo , Lipopolisacáridos/farmacología , Masculino , Área Preóptica/efectos de los fármacos , Área Preóptica/metabolismo , Ratas , Ratas Wistar
8.
Nitric Oxide ; 93: 90-101, 2019 12 01.
Artículo en Inglés | MEDLINE | ID: mdl-31604145

RESUMEN

The mechanisms underlying temporomandibular disorders following orofacial pain remain unclear. Hydrogen sulfide (H2S), a newly identified gasotransmitter, has been reported to modulate inflammation. Cystathionine γ-lyase (CSE) is responsible for the systemical production of H2S, which exerts both pro- and antinociceptive effects through inflammation. In the current study, we investigated whether the endogenous H2S production pathway contributes to arousal and maintenance of orofacial inflammatory pain, through the investigation of the effects of a CSE inhibitor, propargyglycine (PAG), in a rat CFA (Complete Freund Adjuvant)-induced temporomandibular inflammation model to mimic persistent pain in the orofacial region. For this, rats received either CFA or saline in the temporomandibular joints (TMJs), and after 3 or 14 days, they received a single injection of PAG or saline and were evaluated for nociception with the von Frey and formalin test. Also, pro-inflammatory cytokines, tumor necrosis factor-α (TNF-α), and interleukin-1ß (IL-1ß) were analyzed in TMJs and trigeminal ganglion (TG). In this last one, glial cells reactivity was also verified. Endogenous H2S production rate were measured in both, TMJ and TG. Our results indicated decreased allodynia and hyperalgesic responses in rats submitted to CFA after injection of PAG. Moreover, PAG inhibited leucocyte migration to temporomandibular synovial fluid after 3 and 14 days of inflammation. PAG was able to reduce levels of CBS, CSE, TNF-α, and IL-1ß in the TMJ and TG, after 13 days of CFA injection. The observed increased activation of glial cells in the trigeminal ganglia on the 14th day of inflammation can be prevented by the highest dose of PAG. Finally, CBS and CSE expression, and endogenous H2S production rate in the TMJ and TG was found higher in rats with persistent temporomandibular inflammation compared to rats injected with saline and PAG was able to prevent this elevation. Our results elucidated the molecular mechanisms by which H2S exerts its pro-inflammatory and pro-nociceptive role in the orofacial region by alterations in both local tissue and TG.


Asunto(s)
Alquinos/uso terapéutico , Glicina/análogos & derivados , Sulfuro de Hidrógeno/metabolismo , Hiperalgesia/tratamiento farmacológico , Inflamación/metabolismo , Dolor/tratamiento farmacológico , Articulación Temporomandibular/metabolismo , Animales , Cistationina gamma-Liasa/antagonistas & inhibidores , Inhibidores Enzimáticos/uso terapéutico , Glicina/uso terapéutico , Interleucina-1beta/metabolismo , Masculino , Neuroglía/efectos de los fármacos , Ratas Wistar , Ganglio del Trigémino/citología , Ganglio del Trigémino/metabolismo , Factor de Necrosis Tumoral alfa/metabolismo
9.
Respir Physiol Neurobiol ; 263: 38-46, 2019 05.
Artículo en Inglés | MEDLINE | ID: mdl-30831241

RESUMEN

Hydrogen sulfide (H2S) is classically known for its toxic effects. More recently H2S has been documented as a neuromodulator. Here we investigated the central effects of aminooxyacetate (AOA; inhibitor of the H2S-synthesizing enzyme cystathionine ß-synthase, CBS) on cardiovascular, respiratory and thermoregulatory responses to hypercapnia in spontaneously hypertensive rats (SHR). To attain this goal we measured mean arterial pressure (MAP), heart rate (HR), ventilation (VE), and deep body temperature (Tb) of SHR and (normotensive) Wistar Kyoto (WKY) rats before and after microinjection of AOA (9 nmol/µL) or saline into the fourth ventricle immediately followed by 30-min hypercapnia exposure (7% inspired CO2). In saline-treated WKY rats, hypercapnia caused an increase in MAP accompanied by bradycardia, an increase in VE, and a drop in Tb. In AOA-treated WKY rats exposed to hypercapnia, the drug did not affect the increased MAP, potentiated the bradycardic response, attenuated the increased VE, and potentiated the drop in Tb. In saline-treated SHR, in comparison to the saline-treated WKY rats, hypercapnia elicited a minor, shorter-lasting increase in MAP with no changes in HR, evoked a greater increase in VE, and did not induce a drop in Tb. In AOA-treated SHR exposed to hypercapnia, the drug did not change the hypercapnia-induced cardiovascular and ventilatory responses while permitted a drop in Tb. Our findings indicate that AOA, an inhibitor of H2S production, modulates cardiorespiratory and thermoregulatory responses to hypercapnia in normotensive rats, whereas hypertension development in SHR is accompanied by suppression of the AOA effect on the cardiovascular and respiratory responses.


Asunto(s)
Ácido Aminooxiacético/farmacología , Presión Arterial , Regulación de la Temperatura Corporal , Temperatura Corporal , Inhibidores Enzimáticos/farmacología , Frecuencia Cardíaca , Sulfuro de Hidrógeno/antagonistas & inhibidores , Hipercapnia/fisiopatología , Frecuencia Respiratoria , Ácido Aminooxiacético/administración & dosificación , Animales , Presión Arterial/efectos de los fármacos , Presión Arterial/fisiología , Temperatura Corporal/efectos de los fármacos , Temperatura Corporal/fisiología , Regulación de la Temperatura Corporal/efectos de los fármacos , Regulación de la Temperatura Corporal/fisiología , Modelos Animales de Enfermedad , Inhibidores Enzimáticos/administración & dosificación , Frecuencia Cardíaca/efectos de los fármacos , Frecuencia Cardíaca/fisiología , Masculino , Ratas , Ratas Endogámicas SHR , Ratas Endogámicas WKY , Frecuencia Respiratoria/efectos de los fármacos , Frecuencia Respiratoria/fisiología
10.
Free Radic Biol Med ; 129: 186-193, 2018 12.
Artículo en Inglés | MEDLINE | ID: mdl-30243702

RESUMEN

Physical exercise induces inflammatory and oxidative markers production in the skeletal muscle and this process is under the control of both endogenous and exogenous modulators. Recently, molecular hydrogen (H2) has been described as a therapeutic gas able to reduced oxidative stress in a number of conditions. However, nothing is known about its putative role in the inflammatory and oxidative status during a session of acute physical exercise in sedentary rats. Therefore, we tested the hypothesis that H2 attenuates both inflammation and oxidative stress induced by acute physical exercise. Rats ran at 80% of their maximum running velocity on a closed treadmill inhaling either the H2 gas (2% H2, 21% O2, balanced with N2) or the control gas (0% H2, 21% O2, balanced with N2) and were euthanized immediately or 3 h after exercise. We assessed plasma levels of inflammatory cytokines [tumor necrosis factor-α (TNF-α), interleukin (IL)-1ß and IL-6] and oxidative markers [superoxide dismutase (SOD), thiobarbituric acid reactive species (TBARS) and nitrite/nitrate (NOx)]. In addition, we evaluated the phosphorylation status of intracellular signaling proteins [glycogen synthase kinase type 3 (GSK3α/ß) and the cAMP responsive element binding protein (CREB)] that modulate several processes in the skeletal muscle during exercise, including changes in exercise-induced reactive oxygen species (ROS) production. As expected, physical exercise increased virtually all the analyzed parameters. In the running rats, H2 blunted exercise-induced plasma inflammatory cytokines (TNF-α and IL-6) surges. Regarding the oxidative stress markers, H2 caused further increases in exercise-induced SOD activity and attenuated the exercise-induced increases in TBARS 3 h after exercise. Moreover, GSK3α/ß phosphorylation was not affected by exercise or H2 inhalation. Otherwise, exercise caused an increased CREB phosphorylation which was attenuated by H2. These data are consistent with the notion that H2 plays a key role in decreasing exercise-induced inflammation, oxidative stress, and cellular stress.


Asunto(s)
Antiinflamatorios/farmacología , Antioxidantes/farmacología , Hidrógeno/farmacología , Músculo Esquelético/efectos de los fármacos , Estrés Oxidativo/efectos de los fármacos , Especies Reactivas de Oxígeno/antagonistas & inhibidores , Administración por Inhalación , Animales , Proteína de Unión a Elemento de Respuesta al AMP Cíclico/sangre , Proteína de Unión a Elemento de Respuesta al AMP Cíclico/genética , Glucógeno Sintasa Quinasa 3 beta/sangre , Glucógeno Sintasa Quinasa 3 beta/genética , Interleucina-1beta/antagonistas & inhibidores , Interleucina-1beta/sangre , Interleucina-1beta/genética , Interleucina-6/antagonistas & inhibidores , Interleucina-6/sangre , Interleucina-6/genética , Isoenzimas/sangre , Isoenzimas/genética , Masculino , Músculo Esquelético/metabolismo , Músculo Esquelético/fisiopatología , Nitratos/antagonistas & inhibidores , Nitratos/sangre , Nitritos/antagonistas & inhibidores , Nitritos/sangre , Condicionamiento Físico Animal/métodos , Esfuerzo Físico/efectos de los fármacos , Ratas , Ratas Wistar , Especies Reactivas de Oxígeno/sangre , Carrera , Superóxido Dismutasa/sangre , Superóxido Dismutasa/genética , Sustancias Reactivas al Ácido Tiobarbitúrico/metabolismo , Factor de Necrosis Tumoral alfa/antagonistas & inhibidores , Factor de Necrosis Tumoral alfa/sangre , Factor de Necrosis Tumoral alfa/genética
11.
Physiol Behav ; 188: 128-133, 2018 05 01.
Artículo en Inglés | MEDLINE | ID: mdl-29425970

RESUMEN

Hydrogen sulfide (H2S) is an endogenous neuromodulator produced mainly by the enzyme cystathionine gamma-lyase (CSE) in peripheral tissues. A pronociceptive role of endogenously produced H2S has been previously reported by our group in a model of orofacial inflammatory pain. Using the established persistent orofacial pain rat model induced by complete Freund's adjuvant (CFA) injection into temporomandibular joint (TMJ), we have now investigated the putative role of endogenous H2S modulating hypernociceptive responses. Additionally, plasmatic extravasation on TMJ was measured following different treatments by Evans blue dye quantification. Thus, rats were submitted to Von Frey and Formalin tests in orofacial region before and after pharmacological inhibition of the CSE-H2S system combined or not with CFA-induced TMJ inflammation. Pretreatment with CSE inhibitor, propargylglycine (PAG; 88.4 µmol/kg) reduced temporomandibular inflammatory pain when injected locally as well as systemically. In particular, local PAG injection seems to be more effective for hypernociceptive responses in orofacial persistent inflammation since its action is evidenced in the majority analyzed periods of the inflammatory process compared to its systemic use. Moreover, local injection seems to act on temporomandibular vascular permeability, evidenced by decreased plasmatic extravasation induced by local PAG administration. Our data are consistent with the notion that the endogenous synthetized gas H2S modulates persistent orofacial pain responses revealing the pharmacological importance of the CSE inhibitor as a possible therapeutic target for their control.


Asunto(s)
Cistationina gamma-Liasa/metabolismo , Dolor Facial/enzimología , Dolor Facial/etiología , Inflamación/complicaciones , Inflamación/patología , Articulación Temporomandibular/patología , Alquinos/uso terapéutico , Análisis de Varianza , Animales , Inhibidores Enzimáticos/uso terapéutico , Dolor Facial/complicaciones , Dolor Facial/tratamiento farmacológico , Adyuvante de Freund/toxicidad , Glicina/análogos & derivados , Glicina/uso terapéutico , Hiperalgesia/tratamiento farmacológico , Hiperalgesia/etiología , Inflamación/inducido químicamente , Masculino , Dimensión del Dolor , Ratas , Ratas Wistar , Factores de Tiempo , Resultado del Tratamiento
12.
Appetite ; 107: 79-85, 2016 Dec 01.
Artículo en Inglés | MEDLINE | ID: mdl-27460937

RESUMEN

History of sodium depletion cross-sensitizes the effects of drugs of abuse. The objective of the present study was to find out if history of sodium depletion also cross-sensitizes a natural reward such as sugar intake in the rat. Sodium depletion was induced by furosemide combined with removal of ambient sodium for 24 h; it was repeated seven days later. The depletion was immediately followed by 0.3 M NaCl intake in a sodium appetite test (active sodium repletion). Seven days after the last depletion, hydrated and fed (need-free) sucrose-naïve animals were offered 10% sucrose in a first 2-h sucrose test. The sucrose test was repeated once a day in a series of five consecutive days. History of sodium depletion enhanced sucrose intake in the first and second tests; it had no effect from the third to fifth sucrose test. The effect on the initial sucrose intake tests disappeared if the rats did not ingest 0.3 M NaCl in the sodium appetite test. Prior experience with sucrose intake in need-free conditions had no effect on sodium appetite. History of intracellular dehydration transiently influenced sucrose intake in the first sucrose test. We found no evidence for thirst sensitization. We conclude that history of dehydration, particularly that resulting from sodium depletion, combined to active sodium repletion, produced short-term cross-sensitization of sucrose intake in sucrose-naïve rats. The results suggest that the cross-sensitization of sucrose intake related with acquisition of sugar as a novel nutrient rather than production of lasting effects on sugar rewarding properties.


Asunto(s)
Dieta Hiposódica , Azúcares de la Dieta/administración & dosificación , Cloruro de Sodio Dietético/administración & dosificación , Sodio en la Dieta/administración & dosificación , Animales , Apetito , Deshidratación , Furosemida/administración & dosificación , Masculino , Ratas , Ratas Sprague-Dawley , Sed
13.
Blood ; 107(5): 2192-9, 2006 Mar 01.
Artículo en Inglés | MEDLINE | ID: mdl-16249380

RESUMEN

It has been shown that in vivo and in vitro treatment with G-CSF induces the generation of low-density granulocytes (LDGs), which copurify with PBMCs and inhibit IFN-gamma production by human T cells. These results prompted us to postulate an immunomodulatory role for LDGs in acute graft-versus-host disease (aGVHD). Here it is shown that in the mouse experimental model, in vivo and in vitro G-CSF treatment generates LDGs capable of inhibiting 80% of T-cell IFN-gamma production. To assess the role of these LDGs in aGVHD, lethally irradiated (C57BL/6 x BALB/c) F1 hosts were reconstituted with T cell-depleted bone marrow cells plus nylon wool-purified spleen cells from G-CSF-treated (G-NWS) or -nontreated (NWS) C57BL/6 donors. Recipients of G-NWS had a 75% survival rate in contrast to a rate of 25% in the NWS recipients. The protective effect was completely abolished, and the mortality rate was 100% if donor-cell infusion was treated with anti-Gr1. Moreover, if LDGs were infused with NWS, full protection of aGVHD was observed, and no signs of disease were evidenced by mortality rate, weight loss, or histopathology of target organs. These results revealed the unexpected immunosuppressive capacity of G-CSF based on the generation of LDGs, leading to the possibility of using these cells as inhibitors of aGVHD.


Asunto(s)
Trasplante de Médula Ósea , Enfermedad Injerto contra Huésped/prevención & control , Factor Estimulante de Colonias de Granulocitos/farmacología , Granulocitos/trasplante , Enfermedad Aguda , Animales , Femenino , Enfermedad Injerto contra Huésped/patología , Humanos , Depleción Linfocítica/métodos , Ratones
SELECCIÓN DE REFERENCIAS
DETALLE DE LA BÚSQUEDA