# Qishen Yiqi Dropping Pills Protect Against Myocardial Infarction in Mice via Activating SIRT3/FOXO3a Signaling Pathway

## TL;DR

This study shows that Qishen Yiqi Dropping Pills protect mice from heart damage after a heart attack by boosting a key cellular pathway.

## Contribution

The study reveals that QSYQ protects the heart by activating the SIRT3/FOXO3a pathway, a novel mechanism for its therapeutic effects.

## Key findings

- QSYQ improved heart function and reduced infarct size in mice after myocardial infarction.
- QSYQ attenuated oxidative stress and restored antioxidant enzyme levels via the SIRT3/FOXO3a pathway.
- Blocking SIRT3 eliminated the protective effects of QSYQ, confirming its role in the mechanism.

## Abstract

Background: Myocardial infarction (MI) is the leading cause of morbidity and mortality globally. A major pathological progression of MI is the excess generation of reactive oxygen species (ROS), which results in oxidative stress and damage to the ischemic heart. Because damage to the myocardium is irreversible, the development of new therapeutic agents that can decrease the degree of ischemic damage following MI is crucial. The traditional Chinese medicine formulation, Qishen Yiqi dropping pills (QSYQ), has been clinically used in the treatment of various cardiovascular diseases; however, the precise mechanisms underlying its therapeutic effects remain unelucidated. Methods: In this study, we established murine models of MI via coronary artery ligation to investigate the protective effects and mechanisms of QSYQ following MI. Results: The administration of QSYQ significantly improved cardiac function, reduced infarct size, and attenuated ventricular remodeling in mice that underwent MI. Moreover, MI-induced oxidative stress and downregulated levels of antioxidant enzymes were prevented in mice administered QSYQ via upregulating the SIRT3/FOXO3a signaling pathway. Importantly, pretreatment with a selective SIRT3 inhibitor 3-TYP abolished the cardioprotective effects of QSYQ. Conclusions: Our findings elucidate the role and mechanism of QSYQ in protecting against oxidative damage and restoring redox homeostasis following myocardial infarction. This study provides support for the therapeutic potential of QSYQ in the clinical treatment of myocardial ischemic diseases.