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作 者:刘其锋[1] 李莎莎[1] 吴福荣[1] 何敖林[1]
出 处:《现代中西医结合杂志》2011年第27期3393-3394,共2页Modern Journal of Integrated Traditional Chinese and Western Medicine
摘 要:目的观察转化生长因子-β1(TGF-β1)诱导的NRK-52E转分化过程中转分化标志物α平滑肌肌动蛋白(α-SMA)的表达情况及曲尼司特对其的影响。方法 NRK-52E经培养传代后随机分为阴性对照组,TGF-α1诱导组和不同剂量曲尼司特干预组,采用流式细胞仪测定α-SMA(+)细胞的百分数,Western-blot分析细胞表达α-SMA的程度。结果流式细胞术分析显示阴性对照组α-SMA阳性细胞百分比明显增多,说明细胞发生EMT;曲尼司特干预组细胞表达α-SMA阳性细胞百分比呈剂量依赖性递减,且与阳性对照组比较有显著性差异(P<0.05);Western-blot结果也表明,曲尼司特能剂量依赖性降低NRK-52E胞质α-SMA表达的程度。结论曲尼司特可以抑制肾小管上皮细胞α-SMA的表达,从而抑制EMT,减少ECM的积聚,保护肾脏。Objective It is to observe the expression of α-SMA during the EMT of NRK-52E cells induced by TGF-β1 and the effect of tranilast on expression of α-SMA.Methods The NRE-52E cells by cultured were divided into five groups: the negative control group;the cells treated with TGF-β1;the cells treated with TGF-β1 and 100,200,400 mg/L tranilast,and the positive percent of the NRK-52E cells were measured by flow cytometry,and the expression of α-SMA was evaluated by Western Blot.Results The expressions of α-SMA in NRK-52E cells was up-regulated,showing the EMT;and the treatment groups of tranilast were down-regulated dose-dependently by flow cytometry and Western Blot.Conclusion Tranilast has protective effect on NRK-52E cell induced by TGF-β1,of which the mechanism maybe inhibit of EMT through decreasing the expression of α-SMA.
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