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目的 探讨八肽胆囊收缩素 (CCK 8)对肿瘤坏死因子 (TNF) α诱导的大鼠滑膜细胞增生的影响及其可能的分子机制。方法 通过噻唑蓝 (MTT)比色法检测不同浓度的CCK 8对TNF α诱导的大鼠滑膜细胞株RSC 36 4细胞、Ⅱ型胶原性关节炎 (CIA)大鼠滑膜细胞增生的作用 ;用酶联免疫吸附 (ELISA)法测定CCK 8对TNF α作用下RSC 36 4细胞对白细胞介素 (IL) 6分泌的影响。结果 在TNF α存在的情况下 ,10 -6、10 -7和 10 -8mol/L浓度的CCK 8对RSC 36 4细胞和CIA大鼠滑膜细胞的增生有显著的抑制作用 ,而 10 -6mol/L浓度的CCK 8对RSC 36 4细胞IL 6的产生则呈剌激作用 ,CCK的受体拮抗剂丙谷胺可拮抗CCK 8对IL 6产量的促进作用。结论 CCK 8在TNF α存在的情况下可抑制大鼠滑膜细胞株RSC 36 4细胞和CIA大鼠滑膜细胞的增生 ,这种抑制作用可能是通过促进IL 6的产生实现的。提示CCK 8可能具有潜在的调控类风湿关节炎发病过程的作用。
Objective To investigate the effects of cholecystokinin octapeptide (CCK 8) on the proliferation of rat synovial cells induced by tumor necrosis factor α (TNF α) and its possible molecular mechanism. Methods MTT assay was used to detect the effects of different concentration of CCK 8 on synovial cell proliferation induced by TNFα in rat synovial cell line RSC 36 4 and type Ⅱ collagen induced arthritis (CIA). The effect of CCK 8 on the secretion of interleukin (IL) 6 by RSC 36 4 cells treated with TNFα was measured by enzyme-linked immunosorbent assay (ELISA). Results In the presence of TNFα, CCK 8 concentrations of 10 -6, 10 -7 and 10 -8 mol / L significantly inhibited the proliferation of synovial cells in RSC 36 4 cells and CIA rats, whereas 10 -6 mol / L concentration of CCK 8 stimulated the production of IL 6 in RSC 36 4 cells, whereas CCK, a receptor antagonist, proglumide antagonized the promotion of IL 6 production by CCK 8. Conclusions CCK 8 can inhibit the proliferation of synovial cells in synovial cell line RSC 36 4 and CIA rats in the presence of TNFα, which may be through the promotion of IL 6 production. It is suggested that CCK 8 may have a potential role in regulating the pathogenesis of rheumatoid arthritis.