中文摘要：

目的研究锌离子对转化生长因子-β1（TGF-β1）诱导的肾小管上皮细胞转分化（EMT）的影响。方法常规培养肾小管上皮细胞、传代、分组：①正常对照组;②TGF-β1组（10ng/ml TGF-β1作用48h）;③ZnSO4作用组（30μM ZnSO4作用24h后,加10ng/ml TGF-β1作用48h）。采用相差显微镜观察各组细胞表型改变,免疫荧光及Western blotting方法检测波形蛋白（vimentin）、上皮钙黏素（E-cadherin）、Ⅰ型胶原酶（collagenⅠ）蛋白表达。应用Western blotting检测p-Akt蛋白表达。结果 TGF-β1可以导致肾小管上皮细胞vimentin、collagenⅠ和p-Akt蛋白表达增高,使E-cadherin蛋白表达降低。ZnSO4作用后可有效降低由TGF-β1导致的肾小管上皮细胞vimentin、collagenⅠ及p-Akt的高表达,同时使E-cadherin蛋白表达增多。结论 ZnSO4阻抑TGF-β1所致的肾小管上皮细胞的EMT,其作用可能与PI-3K/Akt信号通路相关。

英文摘要：

Objective To investigate that the effect of Zn^2＋ on transforming growth factor-β1（TGF-β1）-induced epithelial-to-mesenchymal transition（EMT）in rat kidney tubular epithelial cells（NRK-52 E cells）.Methods NRK-52 E cells were cultured in a 5% CO2 atmosphere in complete Dulbecco＇s modified Eagle＇s medium（DMEM;low glucose）and the cells were classified into the following three groups：normal control group,TGF-β1 group（10ng/ml TGF-β1 treatment for 48 hours）,TGF-β1/ZnSO4 group（30μM ZnSO4 sulfate pre-treatment followed by 10ng/ml TGF-β1）.The expression of vimentin,E-cadherin,collagen I and P-Akt was detected by immunofluorescence staining or Western blotting.Results TGF-β1 significantly increased the expression levels of vimentin and collagen I and p-Akt,but ameliorated expression level of E-cadherin in NRK-52 E cells.However,pretreatment of Zn SO4 downregulaed TGF-β1-induced overexpression of vimentin and collagen I and p-Akt,and upregulated TGF-β1-induced downexpression of E-cadherin in NRK-52 E cells.Conclusion The inhibition of Zn SO4 on EMT in TGF-β1-induced NRK-52 E cells might be related to PI-3K/Akt pathways.