痹痛康丸对类风湿关节炎大鼠血清自由基的抑制作用  

EFFECT OF BITONGKANG ON THE INHIBITION OF FREE RADICAL IN SERUM OF RATS RHEUMATOID ARTHRITIS

作　　者：闫美荣[1] 侯金凤[1] 闫晓红[1] 吕新亮[2] 

机构地区：[1]内蒙古医学院细胞生物学教研室,内蒙古呼和浩特010059 [2]武警内蒙古总队医院

出　　处：《内蒙古医学院学报》2004年第3期163-165,共3页Acta Academiae Medicinae Neimongol

摘　　要：目的 :进一步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 ( Freund’s)完全佐剂诱导大鼠佐剂性关节炎 ( AA) ,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 :痹痛康治疗组均比模型组 SOD活性升高、LPO含量降低 ,同时使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 ,具有良好的消炎作用 ;抑制氧自由基对组织的炎症损伤 ,痹痛康具有抗氧化作用 ,即能调节活性氧产生和清除之间平衡 ,对佐剂性关节具有明显的治疗作用。Objective: To further explore the pharmacological action and mechanism of Bitongkang pill (BTKP) in treating rheumatoid arthritis(RA). Methods: The Wistar rat with adjuvant arthritis were induced by complete Freund's adjuvant. The changes of the pathologic and the changes of activities and contents of SOD and LPO were observed. Results: As compared with model groups, SOD was markedly raised in BTKP group, LPO was significantly lowered in BTKP group, Simultaneously, the changes of the pathologic in treated group were controlled, fresh vein was decrease, inflammation was lightened, synovial membrane tissues become thin. Conclusion: The BTKP can inhibit synovial membrane inflammation and angiogenesis that has good antiinflammatory function and can inhibit injury of inflammation caused by oxygen free radical. It may be one of the mechanisms of anti-oxidation that BTKP regulate the balance of activated oxygen produce and scavenging. The BTKP have obviously curative effect on rheumatoid 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]