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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-6mRNA表达及核因子NF-κB的影响及其可能的受体机制。方法:大鼠滑膜细胞株RSC -364经TNF-α(10μg/L)、sCCK-8(10-8-10-6mol/L)、CCK受体拮抗剂丙谷胺(2 mg/L)及溶剂单独或联合孵育3 h,用RT-PCR检测细胞IL-6、CCK-AR及CCK-BR mRNA的表达,孵育1 h,用电泳迁移率检测NF-κB活性,孵育30min,用Western blot-ting检测胞浆IκB蛋白表达。结果:RSC -364细胞固有表达CCK-A/B受体,sCCK-8(10-8-10-6mol/L)使IL-6、CCK-AR和CCK-BR mRNA表达进一步增高,明显增加TNF-α诱导的NF-κB活性,降低胞浆中IκB蛋白水平,并可被丙谷胺所拮抗。结论:sCCK-8通过NF-κB途径上调TNF-α诱导的大鼠滑膜细胞IL-6 mRNA表达,此作用可能通过滑膜细胞上的CCK受体实现,提示CCK-8在类风湿性关节炎(RA)发病过程中可能具有调控作用。
OBJECTIVE: To observe the effect of sCCK-8 on the expression of TNF-α-induced RSC-364 IL-6 mRNA and NF-κB in rat synovial cell line and its possible receptor mechanism. Methods: The synovial cell line RSC-364 was induced by TNF-α (10μg / L), sCCK-8 (10-8-10-6mol / L) and CCK receptor antagonist valproic acid And the solvent alone or in combination for 3 h. The expression of IL-6, CCK-AR and CCK-BR mRNA was detected by RT-PCR and incubated for 1 h. The activity of NF-κB was detected by electrophoretic mobility, incubated for 30 min, -ting to detect cytoplasmic IκB protein expression. Results: Expression of IL-6, CCK-AR and CCK-BR mRNA in RSC-364 cells was significantly higher than that in CCK-A / B recipients and sCCK-8 -αinduced the activity of NF-κB, decreased the level of IκB protein in cytoplasm, and antagonized by proglumide. Conclusions: sCCK-8 up-regulates TNF-α-induced IL-6 mRNA expression in rat synovial cells through NF-κB pathway, which may be mediated by CCK receptors on synovial cells, suggesting that CCK-8 is associated with rheumatoid arthritis Inflammation (RA) may play a regulatory role in the pathogenesis.