RESUMO
In this study, an experimental challenge was carried out by feeding Nero Siciliano pigs with acorn to evoke melanin-like pigmentation and support the hypothesis that it is caused by ingested material. Twelve pigs were studied, 6 fed with acorns and 6 fed commercial feed. At slaughter, all the animals fed on acorns showed black discolouration of almost all lymph nodes. The lymph nodes were normal in size and shape. Histochemical tests performed on tissues allowed us to identify and differentiate the pigment. Immunohistochemical staining for macrophage markers showed macrophages containing a variable amount of melanin-like granules. Our data, and the well-known steps of melanin formation, confirm that swine enzymes could act on phenolic substances found in acorns.
Assuntos
Linfonodos/patologia , Doenças Metabólicas/veterinária , Transtornos da Pigmentação/veterinária , Quercus/química , Sementes/efeitos adversos , Ração Animal/análise , Animais , Dieta/veterinária , Transtornos da Pigmentação/induzido quimicamente , Pigmentos Biológicos/química , Sementes/química , Suínos , Doenças dos SuínosRESUMO
OBJECT: Results of recent studies indicate that erythropoietin (EPO) produces a neuroprotective effect on experimental subarachnoid hemorrhage (SAH). It has been reported that S-100 protein levels increase in cerebrospinal fluid (CSF) after SAH, providing a highly prognostic indication of unfavorable outcome. This study was conducted to validate further the findings of S-100 protein as an index of brain damage and to assess whether treatment with recombinant human EPO (rhEPO) would limit the increase of S-100 protein level in CSF following experimental SAH. METHODS: Thirty-two rabbits were each assigned to one of four groups: Group 1, control; Group 2, SAH; Group 3, SAH plus placebo; and Group 4, SAH plus rhEPO (each group consisted of eight rabbits). The rhEPO and placebo were administered to the rabbits after SAH had been induced, and S-100 protein levels in the CSF of these animals were measured at 24, 48, and 72 hours after the experimental procedure. In each group of animals levels of S-100 protein were compared with the mortality rate, neurological outcome, and neuronal ischemic damage. High S-100 protein levels were found in rabbits in Groups 2 and 3, which exhibited poor neurological status and harbored a high number of damaged cortical neurons. Favorable neurological outcome and significant reductions in total numbers of damaged neurons were observed in animals in Group 4 in which there were significantly lower S-100 protein concentrations compared with animals in Groups 2 and 3 (p < 0.001). CONCLUSIONS: The results of this study support the concept that determination of the S-100 protein level in CSF has prognostic value after SAH. The findings also confirm that rhEPO acts as a neuroprotective agent during experimental SAH.
Assuntos
Eritropoetina/farmacologia , Fármacos Neuroprotetores/farmacologia , Proteínas S100/líquido cefalorraquidiano , Hemorragia Subaracnóidea/líquido cefalorraquidiano , Animais , Encéfalo/efeitos dos fármacos , Encéfalo/patologia , Dano Encefálico Crônico/líquido cefalorraquidiano , Dano Encefálico Crônico/patologia , Humanos , Masculino , Exame Neurológico/efeitos dos fármacos , Neurônios/efeitos dos fármacos , Neurônios/patologia , Coelhos , Proteínas Recombinantes , Hemorragia Subaracnóidea/patologiaRESUMO
Functional studies of the autonomic innervation in the photophores of luminescent fishes are scarce. The majority of studies have involved either the stimulation of isolated photophores or the modulatory effects of adrenaline-induced light emission. The fish skin is a highly complex organ that performs a wide variety of physiological processes and receives extensive nervous innervations. The latter includes autonomic nerve fibers of spinal sympathetic origin having a secretomotor function. More recent evidence indicates that neuropeptide-containing nerve fibers, such as those that express tachykinin and its NK1 receptor, neuropeptide Y, or nitric oxide, may also play an important role in the nervous control of photophores. There is no anatomical evidence that shows that nNOS positive (nitrergic) neurons form a population distinct from the secretomotor neurons with perikarya in the sympathetic ganglia. The distribution and function of the nitrergic nerves in the luminous cells, however, is less clear. It is likely that the chemical properties of the sympathetic postganglionic neurons in the ganglia of luminescent fishes are target-specific, such as observed in mammals.
Assuntos
Sistema Nervoso Autônomo/fisiologia , Peixes/fisiologia , Pele/inervação , Animais , Luminescência , Proteínas Luminescentes , Neuropeptídeo Y/fisiologia , Neurotransmissores/fisiologia , Óxido Nítrico/fisiologia , Óxido Nítrico Sintase Tipo I/fisiologia , Fenômenos Fisiológicos da PeleRESUMO
OBJECTIVE: Erythropoietin (EPO) is a pleiotropic cytokine originally identified for its role in erythropoiesis. Recent studies have demonstrated that EPO and its receptor (EPO-R) are expressed in the central nervous system, where EPO exerts neuroprotective functions. Because the expression of the EPO and EPO-R network is poorly investigated in the central nervous system, the aim of the present study was to investigate whether the resident EPO and EPO-R network is activated in the injured nervous system. METHODS: A well-standardized model of compressive spinal cord injury in rats was used. EPO and EPO-R expression was determined by immunohistochemical analysis at 8 hours and at 2, 8, and 14 days in the spinal cord of injured and noninjured rats. RESULTS: In noninjured spinal cord, weak immunohistochemical expression of EPO and EPO-R was observed in neuronal and glial cells as well as in endothelial and ependymal cells. In injured rats, a marked increase of expression of EPO and EPO-R was observed in neurons, vascular endothelium, and glial cells at 8 hours after injury, peaking at 8 days, after which it gradually decreased. Two weeks after injury, EPO immunoreactivity was scarcely detected in neurons, whereas glial cells and vascular endothelium expressed strong EPO-R immunoreactivity. CONCLUSION: These observations suggest that the local EPO and EPO-R system is markedly engaged in the early stages after nervous tissue injury. The reduction in EPO immunoexpression and the increase in EPO-R staining strongly support the possible usefulness of a therapeutic approach based on exogenous EPO administration.
Assuntos
Eritropoetina/fisiologia , Eritropoetina/uso terapêutico , Receptores da Eritropoetina/fisiologia , Traumatismos da Medula Espinal/tratamento farmacológico , Traumatismos da Medula Espinal/fisiopatologia , Aneurisma/etiologia , Animais , Modelos Animais de Doenças , Regulação da Expressão Gênica , Masculino , Neurônios/fisiologia , Ratos , Ratos Sprague-Dawley , Proteínas Recombinantes , Compressão da Medula Espinal/fisiopatologiaRESUMO
We studied the effect of exogenously administered recombinant human interleukin (IL)-6 on the development of experimental autoimmune orchitis (EAO) in C3H/Hej mice. IL-6 significantly reduced histological signs of EAO and appearance of delayed type hypersensitivity against the immunizing testicular germinal cells. The effect was seen even though the cytokine was administered for only 6 consecutive days and 2 weeks after immunization.
Assuntos
Interleucina-6/farmacologia , Orquite/imunologia , Orquite/prevenção & controle , Animais , Humanos , Interleucina-6/imunologia , Masculino , Camundongos , Camundongos Endogâmicos C3H , Orquite/patologia , Proteínas Recombinantes/imunologia , Proteínas Recombinantes/farmacologia , Fatores de TempoRESUMO
CD30 ligand (CD30L) and its receptor CD30 are members of the tumor necrosis factor (TNF) and TNF receptor superfamilies that play a major role in inflammation and immune regulation. To gain insight into the in vivo role of CD30L/CD30 in inflammatory diseases, we have used carrageenan (CAR)-induced pleurisy in mice, a preclinical model of airway inflammation where type 1 proinflammatory cytokines such as interleukin (IL)-1 and TNF-alpha play a key pathogenic role. The data show that prophylactic treatment with anti-CD30L mAb markedly reduces both laboratory and histological signs of CAR-induced pleurisy. These data suggest involvement of CD30-mediated signals in acute immunoinflammatory pathways induced by CAR.