摘要
目的探讨强的松对胶原诱导性关节炎大鼠的疗效及机制。方法建立Ⅱ型胶原蛋白诱导的大鼠关节炎模型;造模成功后随机分为3组,模型对照组,雷公藤组,强的松组;评估各组大鼠关节炎指数;酶联免疫吸附试验检测大鼠血清肿瘤坏死因子-α及白介素-1β水平;观察大鼠滑膜病理(包括炎性浸润、巨噬A型细胞增生、纤维组织增生)。结果给药16d后,强的松组AI较模型对照组明显降低,差异有统计学意义(P<0.01),直至治疗结束,且优于雷公藤组(P<0.05);与正常对照组比较,模型对照组,雷公藤多甙组、强的松组血清TNF-α及IL-1β水平明显增高(均P<0.01);与模型对照组比较,雷公藤多甙组,强的松组血清TNF-α及IL-1β水平明显下降(均P<0.01);与模型对照组比较,强的松组滑膜炎性细胞浸润和巨噬A型细胞增生减低(P<0.05)。结论强的松可下调CIA大鼠血清TNF-α及IL-1β水平并抑制滑膜炎性细胞浸润和巨噬A型细胞增生,从而缓解CIA。
Objective To explore the therapeutic effect and underlying mechanism of prednisone in collagen Ⅱ-induced arthritis.Methods The arthritis model was induced in all rats by hypodermic injection of collagen Ⅱ and incomplete Freund＇s adjuvant in the tail of rats except that in the normal control group.The SD arthritis rats were randomLy divided into three groups.The severity of arthritis was evaluated by Arthritis Index（AI）,serum IL-1 and TNF-α contents were measured by double antibody sandwich ELISA,and Synovial pathological（include inflammatory infiltration,hyperplasia of type A macrophage,synovial cell and fibrous tissue）were assessed.Results Administered for 16 days,AI of prednisone group was significantly lower compared with the model control group（P 0.01）,and the difference was sustained throughout the treatment period,and have a significantly difference compared with Tripterygium glycosides group（TWP）.The serous TNF-α and IL-1β levels of model group,TWP group,prednisone serum were higher compared with the normal control group（P 0.01）.The serous TNF-α and IL-1β levels of TWP group,prednisone serum were lower significantly compared with the model group.The inflammatory cell infiltration and hyperplasia of type A macrophage of synovial membrane were reduced significantly in the prednisone group compared with the model control group（P 0.05）.Conclusion Prednisone can down-regulate CIA rats serum levels of TNF-α and IL-1β levels and inhibition of synovitis cell infiltration and the macrophage type A cells,thus relieve the CIA.
出处
《中国医药科学》
2012年第23期29-31,共3页
China Medicine And Pharmacy
基金
2011年江苏省常州市卫生局重大科技项目(ZD201108)
