Intermedin attenuates high-glucose exacerbated simulated hypoxia/reoxygenation injury in H9c2 cardiomyocytes via ERK1/2 signaling

Abstract

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 signaling. Conclusion: Intermedin may be a novel therapeutic agent for mitigating diabetic cardiovascular injury in the clinical setting.

Retracted: Intermedin attenuates cardiomyocytes hypoxia‐injury through upregulating long noncoding RNA MALAT1

“…11 Hypoxia/reoxygenation injury of H9c2 cells incubated under high-glucose was remitted by IMD. 12 In a rat model of ischemic heart failure, IMD could effectively remit MI through activation of autophagy. 13 These observations described above suggested the possible protective role of IMD in MI.…”