盐酸青藤碱对家兔骨关节炎关节液IL-1β、PGE_2生成与关节组织结构的影响

Effect of tuduranine hydrochloride on PGE_2 and IL-1β in joint fluid and joint organization in rabbits

目的从关节液细胞因子PGE2与IL-1β生成角度探讨盐酸青藤碱治疗骨关节炎的作用机制。方法取健康家兔以木瓜蛋白酶关节腔注射方法制备骨关节炎模型。模型成立后分别以盐酸青藤碱关节腔注射,并分别设玻璃酸钠、曲安奈德对照。治疗结束后取关节液检测PGE2、IL-1β含量,关节组织进行病理学检查。结果盐酸青藤碱使关节液IL-1β、PGE2含量均有较明显降低,玻璃酸钠主要降低PGE2的含量,曲安奈德降低IL-1β的作用更明显。病理学检查显示治疗各组的关节病变程度均较模型组减轻。玻璃酸钠减轻关节软骨损伤作用明显,曲安奈德减轻滑膜炎症突出,盐酸青藤碱在减轻软骨损伤与滑膜炎症方面均有一定作用。结论盐酸青藤碱可抑制骨关节炎病变中关节液炎性细胞因子PGE2、IL-1β生成,是其减轻软骨损伤与滑膜炎症的作用机制。

Objective To investigate the mechanism of tuduranine hydrochloride in treating osteoarthritis in the production of cytokines PGE2 and IL-1β.Methods The rabbit models of OAs were induced by papain injection of articular cavity,and then,the rabbits were injected tuduranine hydrochloride,sodium hyaluronate and tuduranine hydrochloride respectively into articular cavities.After the treatment,the levals of PGE2 and IL-1β were detected,and the pathological changes of joint organization observed.Results The tuduranine hydrochloride reduced the leval of PGE2 and IL-1β significantly;Sodium hyaluronate reduced the content of PGE2 mainly,while the triamcinolone acetonide reduced the IL-1β.Pathological examination showed that the joint lesions in all treatment groups reduced;the sodium hyaluronate reduced the articular cartilage damage obviously,while the triamcinolone acetonide reduced the synovitis prominently.Conclusion The tuduranine hydrochloride can inhibit production of cytokines PGE2 and IL-1β in articular inflammation,which may be the mechanism of reducing the articular cartilage damage and the synovitis.