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；Western blot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-β1、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。
Influence of interleukin 13 on activity of TGF-β1/Smads signaling pathway in bile duct fibroblasts and the interventional effect of dexamethasone
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.