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|Title:||Efeito da talidomida e da pentoxifilina na produção de mediadores inflamatórios e na patogênese da Encefalomielite Autoimune Experimental (EAE)|
|Keywords:||Encefalomielite autoimune experimental; TNF-a; Pentoxifilina; Talidomida; MEDICINA; PATOLOGIA INVESTIGATIVA; Esclerose múltipla|
|Abstract:||Autoimmune encephalomyelitis (EAE) in Lewis rats is an experimental model of demyelinating inflammatory disease of the human central nervous system (CNS). EAE is widely accepted for study immune-inflammatory mechanisms in the CNS related to multiple sclerosis (MS) due to similar clinic. Tumor necrosis factor alpha (TNF-a) has been reported as a key mediator implicated in the physiopathology of CNS inflammatory process. In the present study two drugs (Thalidomide and pantoxifylline) known as TNF-a inhibitors were used during EAE development in Lewis rats. EAE was induced with inoculation of guinea pig spinal cord homogenate in complete Freunds adjuvante in the footpad on day 0 and rats treaties during 15 days with Thalidomide injected subcutaneous or pentoxifylline injected intraperitoneally. Clinical evaluation was carried out daily and histological analysis (staining with hematoxylin and eosin and Weigert Pal Russel) of brain tissue and spinal cord performed at the end of experiment. Griess method was chosen for determination of NO and enzyme immunoassay (ELISA) for TNF-a and interferon gamma (IFN-g) cytokine plasma levels. Thalidomide caused a significant reduction in neuroinflammation and demyelination within the CNS. Plasma levels of NO, IFN-g and TNF-a also showed marked reduction. Such findings were correlated with improvement of clinical symptoms. 90% of rats treated with thalidomide did not develop EAE. Our experiments showed that pentoxifylline was not effective in the modulation of EAE. The results until suggest that thalidomide interfere strongly with pathogenetic mechanisms of EAE development and production of inflammatory mediators. Such drug may also be considered an important tool for use in the therapeutic schemes of inflammatory demyelinating diseases of the CNS Such as multiple sclerosis|
|Appears in Collections:||TEDE sem arquivo|
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