八肽胆囊收缩素对大鼠滑膜细胞株RSC-364增生的影响及其可能的分子机制

Effects of cholecystokinin octapeptide-8 on the proliferation of rat fibroblast-like synovial cells and its possible molecular mechanism

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 fibroblast like synovial cells in the presence of tumor necrosis factor (TNF) α and its possible molecular mechanism.Methods The effects of CCK 8 on proliferation of rat fibroblast like synovial cells were measured by monotetrazolium (MTT) colourmetric assay and the IL 6 production of the RSC 364 cell line at different concentrations of CCK 8 was detected by enzyme linked immunosorbent assay (ELISA).Results At the concentrations of 10 -6 ,10 -7 and 10 -8 mol/L,CCK 8 significantly inhibited the proliferation of RSC 364 cells and cultured synovial cells of collagen incuced arthritis (CIA) rat in the presence of TNF α,at the concentration of 10 -6 mol/L,CCK 8 stimulated the production of interleukin (IL) 6 of RSC 364 cells,and the stimulating effect of CCK 8 on the IL 6 production was significantly inhibited by CCK receptor antagonist proglumide.Conclusion CCK 8 can inhibit the proliferation of RSC 364 cells and cultured synovial cells of CIA rat in the presence of TNF α and this effect might be mediated by stimulating the IL 6 production.The results suggest that CCK 8 is a possible regulator on the pathogenesis of rheumatoid arthritis.