白芍总苷对EAE大鼠中枢神经系统炎症浸润细胞凋亡及Bcl-2、Bax表达的影响

目的 探讨白芍总苷（TGP）对实验性自身免疫性脑脊髓炎（EAE）大鼠中枢神经系统（CNS）炎症浸润细胞凋亡及Bcl-2、Bax表达的影响.方法 建立大鼠EAE模型,将大鼠随机分为正常对照组、模型组、TGP组、泼尼松组,TGP组免疫后第1天起每天经口灌服白芍总苷悬浊液0.2 g/kg,泼尼松组给予泼尼松,正常对照组、模型组给予同体积生理盐水溶液,第17天处死,病理切片观察CNS炎症细胞浸润情况,TUNEL法检测浸润细胞凋亡情况,免疫组化检测浸润细胞Bcl-2、Bax蛋白的表达.结果 泼尼松组、TGP组与模型组相比,中枢神经系统炎症浸润细胞的数目减少,凋亡率增高.TGP组与模型组相比,Bcl-2表达下降,Bax的表达上调,Bcl-2/Bax的比值下降.泼尼松组与模型组相比,Bcl-2/Bax的比值下降.结论 TGP能减轻EAE的病情,其机制可能是下调Bcl-2的表达,上调Bax蛋白的表达,降低Bcl-2/Bax比值,促进EAE大鼠CNS炎症浸润细胞的凋亡,减少CNS炎症细胞的浸润.

Effects of total glucosides of paeony on apoptosis of inflammatory infiltrating cells and expression of Bcl-2 and Bax in CNS of EAE rats

Objective To observe Bcl--2,Bax expression and apoptosis of inflammatory infiltrating cells in the rats＇ central nervous system （CNS） with experimental autoimmune encephalomyelitis （EAE） after dealing with total glucosides of paeony（TGP）. Methods EAE was induced. The female wistar rats were randomly divided into normal group, model group, TGP group, prednisolone group. From day 1 postimmunization to day 17 postimmunization, the rats in TGP group were treated with TGP suspension（oral, 0.2 g/kg） everyday, the rats in prednisolone group were treated with prednisolone, the rats in model group and normal group were treated with sodium chloride of the same volume. 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 Bcl-2, Bax protein of the inflammatory infiltration cells. Results Compared with the model group, the TGP group and prednisolone group had fewer inflammatory infiltrating cells in CNS, higher apoptotic rate. Compared with the model group, the TGP group had lower expression of Bcl-2 protein, higher expression of Bax protein, and the ratio between Bcl-2 and Bax declined. Compared with the model group, the prednisolone group had lower ratio between Bcl-2 and Bax. Conclusions TGP may reduce the ratio between Bcl-2 and Bax through inhibiting the expression of Bcl-2 and promoting the expression of Bax, which may enhances the apoptotic rate of infiltrating inflammatory cells, reduce the number of inflammatory infiltration cells in the CNS of EAE rat model.