中文摘要：

目的：探讨microRNA-30（miR-30）缓解血管紧张素Ⅱ（AngⅡ）所致足细胞损伤的分子机制。方法：（1）通过皮下埋置渗透压泵,给予小鼠AngⅡ[1 000 ng/（kg·min）×28d]构建肾损伤模型。利用原位杂交及qRT-PCR技术检测小鼠肾小球中miR-30s的表达,运用免疫组化及蛋白印迹检测calcineurin信号重要分子细胞瞬时受体电位阳离子通道蛋白6（TRPC6）,钙调磷酸酶（PPP3CA、PPP3CB、PPP3R1）及活化T细胞核因子（NFATC3）表达。（2）给予miR-30s慢病毒尾静脉注射,观察其对AngⅡ诱导损伤模型的肾脏保护作用。（3）体外研究观察miR-30a高表达能否抑制AngⅡ（10-6mol/L）诱导的足细胞骨架损伤和足细胞凋亡。结果：（1）AngⅡ诱导小鼠肾小球中miR-30s水平下调,并上调TRPC6,激活calcium/calcineurin信号通路;（2）高表达的miR-30s能够抑制AngⅡ导致的calcium/calcineurin信号活化从而缓解AngⅡ诱导的肾小球损伤;（3）miR-30s能够逆转AngⅡ所致足细胞骨架损伤及抑制其凋亡过程。结论：miR-30s具有抑制AngⅡ诱导的足细胞损害作用,其机制可能与抑制calcium/calcineurin信号通路有关。

英文摘要：

Objective： To illuminate the protective role of microRNA-30 s in AngⅡ-induced podocyte injury.Methodology：（ 1） Mice were infused with AngⅡ at a dose of 1 000 ng / kg / min for 28 days with the osmotic mini-pumps implanted subcutaneously. The expression of miR-30 s in mice glomeruli was examined by qRT-PCR and in situ hybrization.The expressions of TRPC6, PPP3CA、 PPP3CB、 PPP3R1 and NFATC3 were tested by western blotting and immunohistochemical.（ 2） To examine the protective effects of miR-30 s in Ang Ⅱ-treated mice,miR-30a-expressing lentivirus or control lentivirus was injected via the tail vein on day 14 during the AngⅡ infusion. The glomerular podocyte damage was evaluated with proteinuria,PAS staining and podocyte apoptosis and foot process effacement were used to measure podocye injury.（ 3） treated miR-30-overexpressed podocyte with 10- 6mol / L AngⅡ,and cytoskeletal injury and cell apoptosis were examined by F-actin staing and Annexin V-flow cytometry. Results：（ 1） Ang II infusion induced the downregulation of miR-30 family and the activation of calcium / calcineurin signaling;（ 2） miR-30 a could inhibit Ang Ⅱ-induced activation of calcium / calcineurin signaling and then relieve AngⅡ-induced podocyte injury;（ 3） Exogenous miR-30 a protected podocytes from Ang Ⅱ-induced cytoskeletal damage and apoptosis in vitro. Conclusion： miR-30 s could protect podocyte from AngⅡ-induced damage likely through calcium / calcineurin signaling inhibition.