【摘要】 目的观察硫酸化八肽胆囊收缩素(CCK-8)对TNF-α诱导大鼠成纤维样滑膜细胞株RSC-364细胞增殖及丝裂原活化蛋白激酶p38(p38 MAPK)活性的影响。方法采用噻唑蓝(MTT)比色法检测细胞增殖;Western blot技术检测p38 MAPK活性。结果TNF-α(50μg/L)孵育5 min,p38 MAPK磷酸化水平升高,15 min达高峰,2 h恢复基础水平;孵育15 min时,p38 MAPK磷酸化程度随其剂量(10、25、50μg/L)的增大而增加。CCK-8(10-10~10-6mol/L)剂量依赖性降低TNF-α诱导的细胞增殖及磷酸化p38 MAPK的激活,此作用可被CR1409和CR2945拮抗。SB203580(10μmol/L)可抑制TNF-α引起的细胞增殖。结论CCK-8通过降低p38 MAPK磷酸化水平而抑制TNF-α激活的RSC-364细胞增殖,该作用可能由CCK-A和CCK-B受体共同介导。更多还原

【Abstract】 Objective To study the effect of cholecystokinin-octapeptide（CCK-8） on the proliferation of fibroblast-like synovial cell line RSC-364 and p38 MAPK activity induced by TNF-α in rat.Methods The proliferation of RSC-364 cells was measured by monotetrazolium（MTT） colourmetric assay and the level of activation of p38 MAPK was deteced by Western blot.Results An increase in p38 MAPK phosphorylation was detected 5 min after TNF-α（（50 μg/L））addition,and reached a plateau at（15 min）,finally returned to the basic level at（2 h）.TNF-α（10,25,（50 μg/L）） increased p38 MAPK phosphorylation in a dose dependent manner at 15 min.CCK-8((10^-10)～(10^-6mol/L))could inhibit the proliferation and the level of phosphorylation of p38 MAPK in a dose dependent manner.Moreover the inhibitory effects were partly reversed by CCK-A receptor specific antagonist CR1409 or CCK-B receptor specific antagonist CR2945.SB203580 inhibited TNF-α-stimulated RSC-364 proliferation.Conclusion CCK-8 inhibited TNF-α-stimulated proliferation by decreasing p38 MAPK phosphorylation in RSC-364 cells,which was mediated through CCK-A receptor or CCK-B receptor.更多还原