CCK-8通过调节κB活性促进大鼠滑膜细胞株RSC-364 IL-6转录  

Cholecystokinin octapeptide promotes IL-6 transcriptional activation by regulating nuclear factor-κB activity in rat synovial cell strain RSC-364

作　　者：赵占胜[1] 金玉怀[2] 丛斌[3] 徐锦荣[1] 姚玉霞[3] 李淑瑾[3] 凌亦凌[1] 

机构地区：[1]河北医科大学病理生理教研室,河北石家庄050017 [2]河北医科大学病原生物学教研室,河北石家庄050017 [3]河北医科大学法医学教研室,河北石家庄050017

出　　处：《基础医学与临床》2006年第2期182-186,共5页Basic and Clinical Medicine

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、sCCK-8、CCK受体拮抗剂丙谷胺及溶剂单独或联合应用孵育3h，用RT-PCR检测细胞IL-6 mRNA的表达。孵育1h，用电泳迁移率检测NF-κB活性，孵育30min，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-αB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。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 factor-roB （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^-6 mol/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.

关 键 词：类风湿性关节炎 缩胆囊素 滑膜细胞 白细胞介素 核因子ΚB 

分 类 号：R593.22[医药卫生—内科学]