【摘要】 目的观察硫酸化八肽胆囊收缩素(sCCK-8)对TNF-α诱导大鼠滑膜细胞株RSC-364 IL-6基因表达的影响及核因子NF-κB活性,以探讨CCK-8对类风湿性关节炎(RA)的调控机制。方法大鼠滑膜细胞株RSC-364经TNF-α、sC-CK-8、CCK受体拮抗剂丙谷胺及溶剂单独或联合应用孵育3 h,用RT-PCR检测细胞IL-6 mRNA的表达,孵育1 h,用电泳迁移率检测NF-κB活性,孵育30 min,用Western blot检测胞浆I-κB蛋白表达。结果sCCK-8(10-8~10-6mol/L)明显增加TNF-α诱导的IL-6 mRNA表达及NF-κB活性,呈剂量依赖性,降低胞浆中I-κB蛋白水平,并可被丙谷胺所拮抗。结论sCCK-8在类风湿性关节炎(RA)发病过程中可能具有调控作用。更多还原

【Abstract】 Objective To investigate the effect of sulfated cholecystokinin octapeptide（CCK-8） on TNF-α induced IL-6 mRNA expression and NF-κB activity in rat fibroblast-like synovial cell strain RSC-364.Methods RSC-364 cells were stimulated with TNF-α in the presence or absence of sCCK-8(10^-8～ 10^-6mol/L) and/or CCK receptor antagonist proglumide（2 mg/L）.The expression of IL-6 mRNA was assayed by reverse transcription polymerase chain reaction（RT-PCR）,and nuclear factorκB（NF-κB） binding activity was analyzed by electrophoretic mobility shift assay（EMSA）.I-κB protein level in the cytoplasma was detected by Western blot.Results sCCK-8,at concentrations from 10^-8mol/L to 10^-6mol/L obviously promoted IL-6 mRNA expression and NF-κB binding activity in a dose-dependent manner.I-κB protein level was inhibited by sCCK-8.The effects of sCCK-8 on NF-κB activity and I-κB protein level were attenuated by CCK receptor antagonist proglumide.Conclusions sCCK-8 promoted TNF-α-induced IL-6 mRNA expression by regulating（NF-κB） activity in rat synovial cell strain RSC-364,and suggested that CCK-8 is a potential regulator in the pathogenesis of rheumatoid arthritis.更多还原