新加糖肾康对高糖环境下人肾小管上皮细胞α―平滑肌肌动蛋白和E―钙黏蛋白影响.docVIP

新加糖肾康对高糖环境下人肾小管上皮细胞α―平滑肌肌动蛋白和E―钙黏蛋白影响.doc

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新加糖肾康对高糖环境下人肾小管上皮细胞α―平滑肌肌动蛋白和E―钙黏蛋白影响

新加糖肾康对高糖环境下人肾小管上皮细胞α―平滑肌肌动蛋白和E―钙黏蛋白影响   摘要:目的 观察新加糖肾康对高糖环境培养下人肾小管上皮细胞(HK-2)α-平滑肌肌动蛋白(α-SMA)和E-钙黏蛋白(E-cadherin)的影响,探讨其防治糖尿病肾间质纤维化的作用机制。方法 含10%胎牛血清1640培养基体外培养HK-2细胞。实验分为空白对照组、高糖组、空白血清组和新加糖肾康低、中、高剂量组。药物干预后,MTT法检测细胞增殖,ELISA检测α-SMA和E-cadherin的含量。结果 与空白对照组比较,HK-2细胞经高糖培养后细胞数量和α-SMA含量显著增加、E-cadherin含量明显降低(P0.05);与高糖组比较,新加糖肾康组α-SMA含量降低、E-cadherin含量增加、细胞增殖受到抑制。结论 新加糖肾康能够抑制肾小管上皮细胞表型转化及细胞增殖,具有防治糖尿病肾间质纤维化的作用。   关键词:新加糖肾康;高糖;人肾小管上皮细胞;表型转化;细胞增殖   DOI:10.3969/j.issn.1005-5304.2016.03.015   中图分类号:R285.5 文献标识码:A 文章编号:1005-5304(2016)03-0054-04   Abstract: Objective To observe he effects of new Tangshenkang on α-SMA and E-cadherin of human renal tubular epithelial cell HK-2 in high concentrations of glucose; To explore the mechanism of new Tangshenkang on the prevention and treatment of diabetic renal fibrosis. Methods The HK-2 cells were cultured and divided into control group, high glucose group, animal serum control group, new Tangshenkang low-, medium-, and high-dosage group. After medicine intervention, cell proliferation was tested by MTT assay, and contents of α-SMA and E-cadherin were observed by ELISA assay. Results Compared with control group, α-SMA of HK-2 cultured with high glucose was much notable, but the content of E-cadherin significantly decreased, with statistical significance (P0.05). The content of α-SMA of HK-2 cultured with new Tangshenkang decreased, and the content of E-cadherin increased; cell proliferation was markedly inhibited in culture medium supernatant of HK-2 cells cultured with high glucose plus new Tangshenkang compared with only high glucose, with statistical significance. Conclusion New Tangshenkang can inhibit cell proliferation and epithelial-myofibroblast transdifferentiation of HK-2 cell induced by high glucose, and prevent the development of diabetic renal fibrosis to a certain extent.   Key words: new Tangshenkang; high glucose; human renal tubular epithelial cell HK-2; epithelial-myofibroblast transdifferentiation; cell proliferation

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