1,25(OH)2D3 ameliorates high glucose-induced podocyte injury via PI3K/p-Akt signalling pathway

VernacularTitle:活性维生素D3通过PI3K/p-Akt信号通路抑制高糖诱导的足细胞损伤
Author: Zhixia SONG ; Yinfeng GUO ; Min ZHOU ; Xiaoliang ZHANG ; Bicheng LIU
Publication Type:Journal Article
Keywords: Calcitriol; Podocyte; High glucose; PI3K/p-Akt signalling pathway
From: Chinese Journal of Nephrology 2016;32(5):358-364
CountryChina
Language:Chinese
Abstract: Objective To investigate the effect of 1,25(OH)2D3 on high glucose induced podocyte injury and its signal transduction mechanism.Methods Differentiated mouse podocytes were exposed to normal glucose,high glucose,and different concentrations of 1,25(OH)2D3 or LY294002 (a selective PI3K inhibitor) for 24 h.PCR and immunofluorescent staining were used to detect nephrin,podocin,and desmin.Western blotting was used to detect protein expression of nephrin,podocin,desmin,PI3K,Akt and p-Akt.Results Compared with high glucose group,1,25(OH)2D3 (100 nmol/L and 1000 nmol/L) significantly up-regulated the expression of podocin and nephrin in podocytes induced by high glucose (P ＜ 0.05).Meanwhile,1,25(OH)2D3 (100 nmol/L) significantly reduced the expression of desmin (P ＜ 0.05).PI3K and p-Akt were obviously reduced in high glucose group.In the presence of 1,25(OH)2D3,the trends were reversed.However the above effects of 1,25(OH)2D3 were abolished when p-Akt was blocked by the PI3K inhibitor LY294002.Conclusions 1,25 (OH)2D3 can inhibit high glucose-induced pedocyte injury through PI3K/p-Akt signaling pathway.