CAJ | 학술논문

目的：观察GPR30受体激动剂G1对高糖诱导的EA．hy926内皮细胞内质网应激（ endoplasmic re-ticulum stress，ERS）的影响。方法选用EA．hy926内皮细胞为研究对象，分为3组：正常对照组（Con，17.51mmol/L葡萄糖）、高糖组（HG，33.3mmol/L葡萄糖）、高糖＋G1组（HG＋G1，HG＋1umol/L G1），利用流式细胞术检测3组细胞凋亡率，Western blot 法检测ERS相关分子Bip、IRE1、PERK及凋亡分子Bax、Bcl-2的表达变化，RT-PCR法检测Bip和CHOP的mRNA表达变化。结果 HG组与Con组比较，细胞凋亡率明显升高（P＜0.01），Bip、IRE1、PERK及凋亡分子Bax表达上调（P＜0.01， P＜0.05或P＜0.001），Bcl-2的表达下调（P＜0.01），Bip mRNA、CHOP mRNA表达上调（P＜0.001及P＜0.01）；HG＋G1组与HG组比较，细胞凋亡率明显降低（P＜0.05），Bip、IRE1、PERK及凋亡分子Bax表达下调（P＜0.05或P＜0.01），Bcl-2的表达上调（P＜0.05），Bip mRNA、CHOP mRNA 表达下调（ P＜0.001及P＜0.01）。结论 GPR30受体激动剂G1可抑制EA．hy926内皮细胞内质网应激。
목적：관찰GPR30수체격동제G1대고당유도적EA．hy926내피세포내질망응격（ endoplasmic re-ticulum stress，ERS）적영향。방법선용EA．hy926내피세포위연구대상，분위3조：정상대조조（Con，17.51mmol/L포도당）、고당조（HG，33.3mmol/L포도당）、고당＋G1조（HG＋G1，HG＋1umol/L G1），이용류식세포술검측3조세포조망솔，Western blot 법검측ERS상관분자Bip、IRE1、PERK급조망분자Bax、Bcl-2적표체변화，RT-PCR법검측Bip화CHOP적mRNA표체변화。결과 HG조여Con조비교，세포조망솔명현승고（P＜0.01），Bip、IRE1、PERK급조망분자Bax표체상조（P＜0.01， P＜0.05혹P＜0.001），Bcl-2적표체하조（P＜0.01），Bip mRNA、CHOP mRNA표체상조（P＜0.001급P＜0.01）；HG＋G1조여HG조비교，세포조망솔명현강저（P＜0.05），Bip、IRE1、PERK급조망분자Bax표체하조（P＜0.05혹P＜0.01），Bcl-2적표체상조（P＜0.05），Bip mRNA、CHOP mRNA 표체하조（ P＜0.001급P＜0.01）。결론 GPR30수체격동제G1가억제EA．hy926내피세포내질망응격。
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.