Eur Rev Med Pharmacol Sci 2019; 23 (3 Suppl): 294-303

DOI: 10.26355/eurrev_201908_18660

Aldose reductase inhibitor Epalrestat alleviates high glucose-induced cardiomyocyte apoptosis via ROS

X. Wang, F. Yu, W.-Q. Zheng

Department of Pharmacy, Weihai Central Hospital, Weihai, China. zhengwenqing369@163.com


OBJECTIVE: To clarify the role of aldose reductase inhibitor (ARI) in the high glucose-induced cardiomyocyte apoptosis and its mechanism.

MATERIALS AND METHODS: In this study, H9c2 cardiomyocytes were employed as objects, high-glucose medium as stimulus, and ARI Epalrestat as a therapeutic drug. The cell apoptosis and activity changes of nitric oxide synthase (NOS), NO, and reactive oxygen species (ROS) were evaluated via Hoechst staining, enzyme-linked immunosorbent assay (ELISA), polymerase chain reaction (PCR), and Western blotting. In addition, the mitochondrial membrane potential was measured via fluorescence counting.

RESULTS: Epalrestat inhibited the activity of AR to improve high glucose-induced oxidative stress in cardiomyocytes, weaken ROS activity, relieve the inhibition on NO activity, alleviate mitochondrial membrane potential damage, reduce the level of high glucose-induced cardiomyocyte apoptosis, and suppress the expression and activity of Caspase-3, thereby preventing high glucose-induced cardiomyocyte apoptosis.

CONCLUSIONS: ARI protects against high glucose-induced cardiomyocyte apoptosis.

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To cite this article

X. Wang, F. Yu, W.-Q. Zheng
Aldose reductase inhibitor Epalrestat alleviates high glucose-induced cardiomyocyte apoptosis via ROS

Eur Rev Med Pharmacol Sci
Year: 2019
Vol. 23 - N. 3 Suppl
Pages: 294-303
DOI: 10.26355/eurrev_201908_18660