Wang Cong-Pin, Wu Yu-Lin
Children Hospital of Soochow University, Suzhou 210000, China.
Zhongguo Zhong Yao Za Zhi. 2006 Jan;31(2):155-8.
To explore the mechanism underlying the treatment of rheumatoid arthritis by Keshiling (KSL) in the rats model of FCA-induced arthritis.
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 (IL-2) secreted by thymus were determined by MTT assay.
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 x 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 x 10(3)), respectively. After administration of KSL in vivo at 540 and 270 mg x 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 of T 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.
KSL possesses the anti-inflammation function.
探讨克痹灵（KSL）对弗氏完全佐剂（FCA）诱导的大鼠关节炎模型类风湿关节炎的治疗机制。
用FCA诱导大鼠实验性关节炎。采用紫外分光光度法评估炎性肿胀足趾中前列腺素E2（PGE2）的含量。用MTT法检测刀豆蛋白A（ConA）和脂多糖（LPS）诱导的淋巴细胞增殖以及胸腺分泌的白细胞介素-2（IL-2）的产生。
结果显示，克痹灵在体内和体外浓度为540和270mg·kg⁻¹时可抑制佐剂性关节炎（AIA）大鼠淋巴细胞增殖及IL-2产生。相同剂量的克痹灵可降低炎性肿胀足趾中PGE2的含量，降低的A值分别为25.6、16.1、10.0（A×10³）。克痹灵在体内以540和270mg·kg⁻¹给药后，T淋巴细胞增殖分别减弱32.1%和31.0%，IL-2产生分别被抑制17.5%和14.0%。而克痹灵在体外给药后，T淋巴细胞增殖抑制率分别降低39.0%和22.1%，IL-2产生分别减少27.3%和18.2%。
克痹灵具有抗炎作用。
