痹痛康丸对类风湿关节炎大鼠血清自由基的抑制作用  

Inhibition function of Bitongkang pill on serum free radical in rats with rheumatoid arthritis

作　　者：吕新亮[1] 闫美荣[2] 侯金凤[2] 闫晓红[2] 黄永凯[1] 

机构地区：[1]武警内蒙古总队医院,内蒙古呼和浩特010031 [2]内蒙古医学院,内蒙古呼和浩特010059

出　　处：《现代中西医结合杂志》2005年第12期1555-1556,共2页Modern Journal of Integrated Traditional Chinese and Western Medicine

摘　　要：目的　探讨痹痛康治疗类风湿关节炎(RA)的药理作用机制。方法　用弗氏(Fre und’s)完全佐剂诱导大鼠佐剂性关节炎,观察病理改变及超氧化物歧化酶(SOD)、血清过氧化脂质(LPO)的含量及活性变化。结果　痹痛康治疗组SOD活性较模型组明显升高(P <0 .0 5 ) ,LPO含量较模型组明显降低(P <0 .0 1) ,同时治疗组病理改变得到控制,可见新生血管减少,炎症减轻,滑膜变薄。结论　痹痛康能够抑制滑膜炎症和血管的形成,对佐剂性关节炎具有较明显的治疗作用。Objective It is to discuss the pharmacological active mechanism of Bitongkang pill (BTKP) on rheumatoid arthritis. Methods The rats were given complete Freund's adjuvant to induce adjuvant arthritis. The pathology changes and the contents and activity changes of SOD and LPO were observed. Results The activity of SOD heightened and the content of LPO lowered more in treatment group than those in model group. Simultaneously, the pathologic changes were improved. It could be seen that fresh blood vessels decreased, inflammations were relieved and synovial membrane became thinner. Conclusion BTKP can inhibit synovial membrane inflammation and formulation of blood vessels. It has obvious treatment action on adjuvant arthritis.

关 键 词：痹痛康 类风湿关节炎 病理改变 超氧化物歧化酶 过氧化脂质 

分 类 号：R593.22[医药卫生—内科学]