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作 者:吴福荣[1] 李莎莎[1] 何敖林[1] 刘其锋[1]
出 处:《交通医学》2010年第5期468-470,共3页Medical Journal of Communications
摘 要:目的:探讨曲尼司特对转化生长因子β1(TGF-β1)诱导大鼠肾小管上皮细胞(NRK-52E)转分化作用的影响及机制。方法:应用TGF-β1刺激NRK-52E,分为阴性对照组,TGF-β1诱导组和不同剂量曲尼司特干预组,用流式细胞仪观察曲尼司特干预后NRK-52E的转分化标志物α-平滑肌肌动蛋白(α-SMA)和E-钙粘蛋白(E-cadherin)的表达情况。结果:在TGF-β1诱导NRK-52E细胞转分化过程中,曲尼司特能剂量依赖性下调α-SMA表达,上调E-cadherin表达,两者表达呈负相关(r=-0.653)。结论:提示曲尼司特在TGF-β1诱导肾小管上皮细胞转分化中发挥保护作用。Objective:To investigate the effect of tranilsat on α-SMA and E-cadherin expression in NRK-52E stimulated with TGF-β1.Methods:The cultured NRK-52E were divided into five groups:(1)the negative control group: cells maintained in DMEM/F12 medium;(2)the cells treated with 8ng/μl TGF-β1;(3)the cells treated with 8ng/μl TGF-β1 and 100 ng/μl tranilast;(4)the cells treat-ed with 8ng/μ TGF-β1 and 200ng/μl tranilast;(5)the cells treated with 8ng/μl TGF-β1 and 400 ng/μl tranilast.The cytometry was used to detect the percentage of α-SMA and E-cadherin positive NRK-52E cells.Result:After TGF-β1 stimulation for 24h,the per-centage of α-SMA positive cells was markedly enhanced,while dose-dependently decreased in tranilast treated groups.On the con-trary,the expression of E-cadherin were markedly decreased in NRK-52E cells induced by TGF-β1,and tranilast dose-dependently in-crease the level of E-cadherin.Conclusion:Transdifferentiation of cultured NRK-52E induced by TGF-β1 can be inhibited by certain level of tranilast.Tranilast may be a potential effective antifibrotic compound in the kidney disease by inhibiting TGF-β1-induced EMT.
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