Inhibitory effect of G1 on the endoplasmic reticulum stress in EA.hy926 endothelial cells
10.3969/j.issn.1005-4847.2014.02.006
- VernacularTitle:G1对 EA．hy926内皮细胞内质网应激的抑制作用
- Author:
Donghui XIA
;
Xingyi CAO
;
Jingyu WANG
;
Ming YUAN
;
Shiwen WU
- Publication Type:Journal Article
- Keywords:
G1;
Endoplasmic reticulum stress;
Atherosclerosis;
EA.hy926 endothelial cells
- From:
Acta Laboratorium Animalis Scientia Sinica
2014;(2):26-31
- CountryChina
- Language:Chinese
-
Abstract:
Objective To observe the effect of GPR30 agonist G1 on high glucose-induced endoplasmic reticulum stress ( ERS) in endothelial EA .hy926 cells.Methods EA.hy926 endothelial cells were divided into three groups:nor-mal control group (Con, 17.51 mmol /L glucose), high glucose (HG, 33.3 mmol /L), high glucose +G1 group (HG+G1, HG +1 μmol/L G1).The apoptosis rate of endothelial cells was measured by flow cytometry , the protein expres-sion changes of ERS related molecules Bip , IRE1, PERK and apoptotic molecules Bax , Bcl-2 were measured by Western blot, the mRNA expressions of Bip and CHOP were measured by RT-PCR assay.Results Compared with Con group , the apoptosis in HG group was significantly increased (P <0.01), Bip, IRE1, PERK and apoptotic molecule Bax were upreg-ulateded (P <0.05, P<0.01 or P <0.001), Bcl-2 downregulatted (P <0.01) and Bip mRNA, CHOP mRNA expres-sion were upregulated (P <0.001 and P<0.01).Compared with the HG group, apoptosis rate in HG +G1 group was significantly lower (P <0.05), BIP, IRE1, PERK and apoptotic molecules Ba.0 downregulated ( P <0.05 or P <0.01), Bcl-2 expressions was increased (P <0.05), Bip mRNA and CHOP mRNA expression were decreased (P<0.001 or P<0.01).Conclusion GPR30 agonist G-1 inhibits EA.hy926 ERS in endothelial cells.
