血管紧张素1-7对高糖诱导人肾小管上皮细胞转分化的影响及其机制

目的 研究血管紧张素1-7（Ang 1-7）对高糖诱导人肾小管上皮细胞（HK-2）转分化的影响及其可能机制。 方法 培养HK-2细胞分组如下：对照组（N组）、高糖组（H组）、高糖+Ang 1-7组（A组）、高糖+Ang 1-7+A779组（D组）、高糖+吡格列酮组（P组）。Western印迹检测各组HK-2细胞过氧化物酶体增殖物激活受体γ（PPAR-γ）及α平滑肌肌动蛋白（α-SMA）的蛋白表达；实时定量PCR检测HK-2细胞PPAR-γ及α-SMA的mRNA表达；免疫荧光检测α-SMA表达。 结果 Ang 1-7可上调高糖刺激下HK-2细胞PPAR-γ蛋白及mRNA表达（P < 0.05）；抑制高糖刺激的α-SMA蛋白及mRNA表达（P < 0.05）。这种作用与PPAR-γ激动剂吡格列酮类似。给予Mas受体抑制剂A779后，Ang 1-7的上述作用可被部分抑制。 结论 Ang 1-7在体外可通过上调PPAR-γ表达，从而部分抑制高糖诱导的α-SMA表达，实现其抑制转分化的作用，而这种作用部分通过Mas受体所介导。

Effect of angiotensin 1-7 on human renal proximal tubular epithelial cell transdifferentiation induced by high glucose and its mechanism

Objective To investigate the effect of angiotensin 1-7 (Ang 1-7) on renal proximal tubular epithelial cell (HK-2) transdifferentiation induced by high glucose. Methods All the raised HK-2 cells were divided into 5 groups: normal control group,high glucose group,high glucose with Ang1-7 group,high glucose with Ang1-7 and A779 group,high glucose with pioglitazone group.Expression of peroxisome proliferator activated receptor-γ (PPAR-γ) and α-smooth muscle actin (α-SMA) was detected by Western blotting,real-time PCR and immunofluorescence.Results The levels of PPAR-γ protein and mRNA in HK-2 cells were significantly increased after treatment with high glucose and Ang 1-7.Expression of α-SMA protein and mRNA was inhibited remarkably after treatment with high glucose and Ang 1-7.These effects of Ang 1-7 on HK-2 cells could be reversed by Mas receptor antagonist A779. Conclusion Ang 1-7 inhibits high glucose-induced expression of o-SMA in HK-2 cells,which is in part through the Mas.