黄芪糖蛋白诱导佐剂性关节炎大鼠体内细胞凋亡的研究

目的:探讨黄芪糖蛋白对佐剂性关节炎大鼠体内细胞凋亡的诱导作用。方法:建立大鼠佐剂性关节炎模型,治疗2周后,取外周血、膝关节滑膜组织,分别使用流式细胞术和原位末端标记(TUNEL)法检测外周血淋巴细胞和膝关节滑膜组织的细胞凋亡情况,使用免疫组织化学法检测膝关节滑膜组织中Fas、FasL的蛋白表达水平。结果:低剂量黄芪糖蛋白可提高外周血CD4+、CD+8细胞的凋亡比例(P<0.05),低、中、高剂量黄芪糖蛋白均可增加膝关节滑膜组织的细胞凋亡率(P<0.01),同时降低Fas表达水平(P<0.01),增强FasL表达水平(P<0.01)。结论:黄芪糖蛋白可诱导佐剂性关节炎大鼠外周血淋巴细胞及膝关节滑膜组织细胞凋亡,且调节滑膜组织中Fas、FasL的蛋白表达水平。

Study on inducing of apoptosis in adjuvant arthritis rats with glycoproteins from astragalus membranaceus

Objective:To study the inducing effect of apoptosis in adjuvant arthritis(AA) rats with GP(glycoprotein from Astragalus membranaceus).Methods:Male rats were randomly divided into 6 groups:normal group,model group,TP(Triptolide) group and GP groups.AA model was established by optimum injecting the complete Freund’s adjuvant(CFA) 0.1ml on the right rear toe.One week later,medcines were given intraperitoneal injection.GP groups were treated with GP at 0.7,3.5,7.0mg/kg body weight every day.TP group rats were administered with TP at 40μg/kg.AA and normal group rats were given normal saline instead.Apoptosis in rats was detected by FCM and TUNEL after two weeks.Expression levels of Fas and FasL in synovium of knee joint were detected by immuno-histochemistry.Results:The flow cytometry showed that low density GP can raise the apoptotic percentage of CD4+ cells and CD8+ cells(P<0.05).The TUNEL labeling demonstrated that all density GP both can improve the apoptotic percentage of synovial cells in knee joint(P<0.01).The immuno-histochemistry displayed that GP can decrease the expression of Fas and enhance the expression of FasL.Conclusion:This study demonstrated that GP can induce apoptosis in AA rats and adjust the expression levels of Fas and FasL.