Empagliflozin Improves Cardiac Function in Rats with Chronic Heart Failure

Author:

Wang Zhenzhen1,Liu Qian1,Wang Xiaofang1,Wang Pengpeng2,Wang Zhuwen1,Zhang Fenglei1

Affiliation:

1. Department of Cardiology, People’s Hospital of Dongying, No. 317, Dong Cheng Nan Yi Road, Dongying, Shandong Province, China

2. Dezhou Municipal Hospital of Shandong Province, China

Abstract

Abstract Objective To examine the effect of empagliflozin on cardiac function in rats with chronic heart failure and the possible mechanism.Methods Forty 6-week-old male SD rats were randomly divided into the control group, empagliflozin treatment group, and sham-operated group. SD rats in the control group and empagliflozin treatment group were subjected to ligation of the anterior descending coronary artery to induce an acute myocardial infarction model. SD rats in the sham-operated group were only subjected to threading of the anterior descending branch of the coronary artery without ligation. On the second day after surgery, the control group and sham operation group were given physiological saline by gavage, while the empagliflozin treatment group was given empagliflozin (30 mg/kg/day) by gavage. Sixteen weeks later, cardiac function, intracellular reactive oxygen species (ROS) levels, mitochondrial membrane potential (MMP), serum brain natriuretic peptide, hypersensitive C-reactive protein (hs-CRP), iNOS expression levels and myocardial morphological changes were observed.Results Compared with that in the control group, heart function in the empagliflozin treated group was significantly improved, MMP was increased, intracellular ROS levels were decreased, and NT -proBNP and hs-CRP were significantly reduced, and HE staining showed that the cell oedema was less than that in the control group, tissue arrangement was more orderly, and iNOS expression was inhibited.Conclusion Empagliflozin can improve cardiac function in rats with chronic heart failure, and the mechanism may involve inhibiting inflammation, reducing myocardial oxidative stress, and improving myocardial fibrosis.

Publisher

Research Square Platform LLC

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