克湿灵治疗类风湿性关节炎的作用机制研究

Study on mechanism underlying the treatment of rheumatoid arthritis by Keshiling

目的:了解克湿灵(KSL)对大鼠佐剂性关节炎动物模型的作用机制。方法:氟氏完全佐剂诱发大鼠佐剂性关节炎;以炎性肿胀足的前列腺素E2含量、细胞因子、淋巴细胞的功能变化作为观察指标;用紫外分光光度法测定炎性肿胀足的前列腺素E2含量,采用MTT法检测胸腺、脾淋巴细胞增殖反应;用活化的小鼠脾淋巴细胞MTT比色法检测胸腺淋巴细胞产生的IL-2的活性。结果:克湿灵高(540 mg.kg-1)、中(270 mg.kg-1)、低(135 mg.kg-1)3个剂量均能降低炎性肿胀足前列腺素E2的含量,其降低的量分别为25.6,16.1,10.0(A×1 000);克湿灵高、中2个剂量组可明显抑制刀豆蛋白A(ConA)诱导的T淋巴细胞增殖反应和IL-2的生成,体内给药对T淋巴细胞增殖反应的抑制率分别为32.1%,31.0%,对IL-2生成的抑制率分别为17.5%,14.0%;体外给药对T淋巴细胞增殖反应的抑制率分别为39.0%,22.1%,对IL-2生成的抑制率分别为27.3%,18.2%;脂多糖(LPS)诱导的B淋巴细胞增殖无明显变化。结论:克湿灵对类风湿性关节炎具有抗炎作用。

Objective： To explore the mechanism underlying the treatment of rheumatoid arthritis by Keshiling （KSL） in the rats model of FCA-induced arthritis. Method： The experimental arthritis was induced by FCA in the rats. The content of PGE2 in the inflammatory swelling toes was evaluated by ultraviolet spectrophotometric method. The ConA and LPS-induced lymphocytes proliferation and the production of interleukin-2 （ID2） secreted by thymus were determined by MTT assay. Result： Results showed that the increases of lymphocyte proliferation and IL-2 production in AIA rats could be inhibited by KSL at the concentrations of 540 and 270 mg·kg^-1 in vivo and vitro. KSL at the same doses decreased the contents of PGE2 in inflammatory swelling toes, and the decreased A values were 25.6,16.1,10.0（ A ×10^3）, respectively. After admirfistration of KSL in vivo at 540 and 270 mg·kg^-1 the T lymphocyte proliferation were attenuated by 32.1% and 31.0%, and the production of IL-2 was inhibited by 17.5% and 14.0% respectively. While the inhibitory rates ofT lymphocyte proliferation were reduced by 39.0% and 22.1% and the production of IL-2 was diminished by 27.3% and 18.2% respectively following the administration of KSL in vitro. Conclusion： KSL possesses the anti-inflammation function.