[Objective]To establish the Wistar-rat model of experimental autoimmune encephalomyelitis(EAE), observe the effects of triptolide(Tri) on EAE .explore NF-kBp65, Bcl-2, Bax expression and apoptosis of inflammatory infiltrating cells in the rats' central nervous(CNS) with EAE after dealing with Tri. [Methods]1 EAE was induced by being injected guinea pig spinal cord homogenate(GPSCH)in complete Freund's adjuvant(CFA) in the four footpads and different concentration bordetella pertussis vaccine(BPV) in one footpad .2 The female wistar rats were randomly divided into control group, EAE groupand Tri group. From day 11 postimmunization to day 28 postimmunization, the rats in Tri group were treated with an intraperitoneal injection of Tri (40 μg/kg-d) , and the rats in control group and EAE group were treated with an intraperitoneal injection of sodium chloride of the same volume. The clinical and histological manifestation of the diseas was observed in each group until 45 days postimmunization .3 Groups and treatment were same to method 2, but the rats wer killed on day 17 postimmunization .The inflammatory infiltration cells in the CNS were counted under the microbioscope and the apoptosis of them were detected by terminal deoxynucleotidyl transferase mediated dUTP nick end labeling (TUNEL). Immunohistochemical staining was used to measure the expression level of NF-kBp65, Bcl-2, Bax protein of the inflammatory infiltration cells.[Results]1 Clinical signs of EAE of rats which were immunized in the four footpads developed on day 11, peaked on day 17 postimmunization(PI)with obvious histological change .The recovery stage lasts about 12 days. Compared with... |