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目的:探讨白细胞介素13(IL-13)对胆管成纤维细胞转化生长因子β1(TGF-β1)/Smads通路活性的影响及地塞米松(Dex)的干预作用.方法:分离、培养兔胆管成纤维细胞并鉴定后分别给予IL-13、IL-13联合不同浓度的Dex(0.01、0.05、0.25 mg/mL)干预48 h,以无处理的胆管成纤维细胞为空白对照,分别用CCK-8细胞计数法测定各组细胞增殖水平;real-time PCR检测各组细胞TGF-β1、Smad3及Smad4基因mRNA表达;Westernblot检测各组细胞TGF-β1及Smad4蛋白表达.结果:与空白对照组比较,在IL-13干预48 h后,胆管成纤维细胞增殖明显加速、TGF-β 1、Smad3及Smad4 mRNA表达均明显上调,TGF-β1、Smad4蛋白表达明显上调(均P＜0.05),而Dex对IL-13引起的上述变化有明显的抑制作用,并呈一定的浓度依赖趋势(部分P＜0.05).结论:IL-13能增加胆管成纤维细胞TGF-β1/Smads通路的活性,削弱该通路的活化可能是Dex抑制良性胆道狭窄形成的机制之一.“,”Objective:To investigate the influence of interleukin 13 (IL-13) on activity of transforming growth factor-β1 (TGF-β1)/Smads signaling pathway in bile duct fibroblasts and the interventional effect of dexamethasone (Dex).Methods:Rabbit bile duct fibroblasts were isolated and cultured and then identified.Then,the bile duct fibroblasts were exposed to IL-13 or IL-13 plus different concentrations (0.01,0.05 and 0.25 mg/mL) of Dex respectively for 48 h,using untreated bile duct fibroblasts as blank control.Afterwards,cell proliferation was assessed by CCK-8,the mRNA expressions of TGF-β1,Smad3 and Smad4 were determined by real-time PCR and the protein expressions of TGF-β1 and Smad4 were examined by Western blot.Results:In bile duct fibroblasts after exposure to IL-13 for 48 h,the cell proliferation was significantly increased,the mRNA expressions of TGF-β1,Smad3 and Smad4 and the protein expressions of TGF-β1 and Smad4 were significantly up-regulated (all P＜0.05),and the above changes exerted by IL-13 were significantly inhibited by Dex addition in a certain concentration-dependent manner (part P＜0.05).Conclusion:IL-13 can enhance the activity of TGF-β1/Smads pathway in bile duct fibroblasts,and weakening the activation of this signaling pathway may be one of the mechanisms of the inhibitory effect of Dex on benign biliary stricture.