European Journal of Inflammation | |
Intermedin attenuates high-glucose exacerbated simulated hypoxia/reoxygenation injury in H9c2 cardiomyocytes via ERK1/2 signaling: | |
HongLi1  | |
关键词: ERK; H9c2; high glucose; hypoxia/reoxygenation; intermedin; | |
DOI : 10.1177/1721727X17744096 | |
学科分类:医学(综合) | |
来源: Sage Journals | |
【 摘 要 】
Objective:This study investigated whether and how intermedin (IMD) exerted a protective effect against simulated hypoxia/reoxygenation (H/R) injury in high-glucose-treated H9c2 cells.Methods:Cellular viability was assessed via 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) assay. Oxidative stress was determined by malondialdehyde and superoxide dismutase content in the culture medium supernatant. Flow cytometry with Annexin V/propidium iodide staining was used to detect the cardiomyocyte apoptosis rate. The protein expression of Bax, Bcl-2, caspase-3, and ERK1/2 was determined by western blot.Results:IMD administration to H9c2 cells during H/R injury decreased oxidative stress product generation and inhibited apoptosis (P < 0.05 or P < 0.01) while these effects were blocked by the ERK1/2 inhibitor (P < 0.05 or P < 0.01). Through the application of a specific ERK1/2 inhibitor, it was demonstrated that IMD mitigates high-glucose-induced oxidative stress and apoptosis via ERK1/2 signa...
【 授权许可】
CC BY-NC
【 预 览 】
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RO201904022301326ZK.pdf | 392KB | download |