1.Salidroside attenuates high glucose-induced rat renal glomerular endothelial cell injury via up-regulating HIF-1α expression
Rui-Yan XIE ; Xue-Ling FANG ; I.RAGE HAMZE ; Tong-Xia CUI ; Wei-Ping ZHU
Chinese Journal of Pathophysiology 2019;35(2):237-242
AIM:To observe the expression of hypoxia-inducible factor-1α (HIF-1α) , vascular endothelial growth factor A (VEGFA) and vascular endothelial cadherin (VE-cadherin) in cultured rat renal glomerular endothelial cells (rRGECs) exposed to glucose at different concentrations in vitro, and to verify the hypothesis that salidroside attenuates high glucose (HG) -induced injury of rRGECs by boosting HIF-1αlevel.METHODS:rRGECs were divided into 4group:normal glucose (NG) group, HG groups, hypertonic group and salidroside+HG group.The viability of rRGECs was measured by MTT assay.The mRNA expression of VEGFA, VE-cadherin and HIF-1αwas detected by RT-qPCR.The protein expression of HIF-1αwas determined by Western blot.RESULTS:Compared with NG group, the mRNA and protein expression of HIF-1αwas increased when the rRGECs were treated with glucose at concentration of 20 mmol/L for 24h (P<0.01).Compared with NG group, the mRNA expression of HIF-1αwas decreased in HG groups for 120 h (P<0.05).Compared with NG group, the mRNA expression of VE-cadherin was significantly down-regulated in HG groups for24 h or 120 h (P<0.05).Compared with NG group, the mRNA expression of VEGFA was increased in HG groups at 24h (P<0.05) , while the mRNA expression of VEGFA was decreased at 120 h (P<0.05).Compared with NG group, no statistical difference in the mRNA expression levels of HIF-1α, VE-cadherin and VEGFA in DM group was observed.Compared with HG group, salidroside promoted the viability of rRGECs (P<0.01) , and up-regulated the mRNA expression of HIF-1αand VE-cadherin, and the protein expression of HIF-1α (P<0.05).CONCLUSION:High glucose regulates HIF-1αexpression in rRGECs in connection with cell viability, the concentration of glucose, the culture time and HIF/VEGF signaling.Salidroside promotes rRGEC growth against high glucose-induced cell apoptosis via up-regulating the expression of HIF-1α.