# Acanthopanax senticosus Saponins Mitigate Left Ventricular Remodelling and Inhibit the Induction of MMP-2, MMP-9 in a Rat Model of Myocardial Infarction

**Authors:** Xinjie Li, Bingshu Quan, Jianpeng Guo

PMC · DOI: 10.3390/ijms27052379 · 2026-03-04

## TL;DR

Acanthopanax senticosus saponins improve heart function and reduce harmful changes after heart attacks in rats.

## Contribution

The study reveals that ASS mitigates ventricular remodelling by inhibiting MMP-2 and MMP-9 expression.

## Key findings

- ASS improved cardiac function and reduced myocardial injury in a rat model of myocardial infarction.
- ASS inhibited the expression of MMP-2 and MMP-9 while increasing TIMP-1 levels.
- ASS reduced inflammation, oxidative stress, and fibrosis markers in the heart.

## Abstract

Acute myocardial infarction can lead to ventricular remodelling, which affects ventricular function and survival prognosis. Therefore, improving ventricular remodelling has become a focus of research. This study aims to investigate the effect of Acanthopanax senticosus leaf saponins (ASS) on cardiac function and left ventricular remodelling in a rat model of myocardial infarction, and explore its potential mechanism. Coronary artery ligation was used to establish a rat model of myocardial infarction, and ASS was administered orally for 28 days. After 28 days, cardiac function was evaluated by hemodynamic detection, and the levels of myocardial enzymes, inflammatory cytokines, oxidative stress and fibrosis-related factors were detected. The degree of fibrosis was evaluated by immunohistochemical detection of collagen I and collagen III deposition. The expression levels of MMP-2, MMP-9 and TIMP-1 were checked by Western blot. Compared with the Sham group, the cardiac function of the Model group was significantly impaired, and ASS administration could improve this change. In addition, compared with the Model group, ASS significantly alleviated myocardial injury, reduced the release of inflammatory cytokines TNF-α and IL-β, improved the oxidative stress state, reduced the release of NT-propBNP, Ang II, ET-1 and inhibited myocardial fibrosis. Moreover, ASS could reduce the expression of MMP-2 and MMP-9, and increase the expression level of TIMP-1. In conclusion, ASS may inhibit left ventricular remodelling by reducing the expression of MMP-2 and MMP-9.

## Linked entities

- **Proteins:** MMP2 (matrix metallopeptidase 2), MMP9 (matrix metallopeptidase 9), TIMP1 (TIMP metallopeptidase inhibitor 1), TNF (tumor necrosis factor), Agt (angiotensinogen), EDN1 (endothelin 1)
- **Diseases:** myocardial infarction (MONDO:0005068)
- **Species:** Rattus norvegicus (taxon 10116)

## Full-text entities

- **Genes:** Agt (angiotensinogen) [NCBI Gene 24179] {aka ANRT, Ang, AngII, PAT}, Mmp2 (matrix metallopeptidase 2) [NCBI Gene 81686], Tnf (tumor necrosis factor) [NCBI Gene 24835] {aka RATTNF, TNF-alpha, Tnfa}, Mmp9 (matrix metallopeptidase 9) [NCBI Gene 81687], Timp1 (TIMP metallopeptidase inhibitor 1) [NCBI Gene 116510] {aka TIMP-1, Timp}, Edn1 (endothelin 1) [NCBI Gene 24323] {aka Et1}
- **Diseases:** myocardial injury (MESH:D009202), inflammatory (MESH:D007249), Left Ventricular Remodelling (MESH:D020257), Myocardial Infarction (MESH:D009203), fibrosis (MESH:D005355)
- **Chemicals:** ASS (-)
- **Species:** Rattus norvegicus (brown rat, species) [taxon 10116]

## Figures

6 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12986085/full.md

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Source: https://tomesphere.com/paper/PMC12986085