Related Experiment Video
Updated: Jun 22, 2026
Improved Rodent Model of Myocardial Ischemia and Reperfusion Injury
Published on: March 7, 2022
Effect of WenXin KeLi on Improvement of Arrhythmia after Myocardial Infarction by Intervening PI3K-AKT-mTOR Autophagy
Meng Lv1, Ding Yang1, Xiaodi Ji1
1Dongzhimen Hospital Affiliated to Beijing University of Chinese Medicine, Key Laboratory of Chinese Internal Medicine of Ministry of Education and Beijing, Beijing 100700, China.
Insights
WenXin KeLi improves cardiac function and reduces arrhythmia risk after myocardial infarction (MI) by activating the PI3K-AKT-mTOR pathway, enhancing autophagy, and increasing connexin43 expression in rats. This study reveals its cardioprotective mechanism against MI-induced complications.
Area of Science:
- Cardiovascular Research
- Pharmacology
- Cellular Biology
Background:
- Myocardial infarction (MI) is a critical cardiovascular condition where post-MI arrhythmia significantly increases sudden cardiac death risk.
- WenXin KeLi, a traditional Chinese medicine, is clinically used to manage arrhythmia and mitigate post-MI risks.
- Understanding WenXin KeLi's cardioprotective pharmacological mechanisms is crucial for its therapeutic application.
Purpose of the Study:
- To investigate the pharmacological mechanism of WenXin KeLi in protecting the heart following myocardial infarction.
- To explore the effects of WenXin KeLi on cardiac autophagy, connexin43 (CX43) expression, and arrhythmia in a rat model of MI.
- To elucidate the role of the PI3K-AKT-mTOR signaling pathway in WenXin KeLi's cardioprotective effects.
Main Methods:
- Establishment of a myocardial infarction (MI) model in rats by ligating the left coronary artery.
- Assessment of ventricular fibrillation threshold (VFT) via electrical stimulation to evaluate arrhythmia susceptibility.
- Measurement of autophagy-related proteins (Beclin1, LC3II/LC3I, P62) and CX43 expression using Western Blot.
- Analysis of the PI3K-AKT-mTOR signaling pathway and CX43 expression in response to WenXin KeLi treatment.
- Evaluation of cardiac structure and function using gross pathology, Masson staining, and echocardiography.
Main Results:
- MI significantly reduced VFT and altered cardiac autophagy markers (increased Beclin1, LC3II/LC3I; decreased P62) and CX43 expression.
- WenXin KeLi treatment increased VFT, improved cardiac structure and function (e.g., increased LVEF, LVFS; decreased LVEDD, LVESD), and normalized collagen deposition.
- WenXin KeLi upregulated the PI3K-AKT-mTOR pathway (increased p-PI3K, p-AKT, p-mTOR) and CX43 expression, while modulating autophagy markers (decreased LC3II/LC3I, Beclin1; increased P62).
Conclusions:
- WenXin KeLi demonstrates significant cardioprotective effects in a rat model of MI, reducing arrhythmia risk.
- The cardioprotection is associated with the activation of the PI3K-AKT-mTOR signaling pathway, modulation of cardiac autophagy, and restoration of CX43 expression.
- These findings support WenXin KeLi's therapeutic potential in managing post-myocardial infarction complications and improving patient outcomes.
Background:
Myocardial infarction (MI) is an acute and serious cardiovascular disease. Arrhythmia after MI can lead to sudden cardiac death, which seriously affects the survival outcome of patients. WenXin KeLi is a Chinese patent medicine for the treatment of arrhythmia in a clinic, which can significantly improve symptoms of palpitation and play an important role in reducing the risk of arrhythmia after MI. In this study, we aimed to explore the pharmacological mechanism of WenXin KeLi in protecting the heart.
Methods:
The MI model was established by ligating the left coronary artery and the ventricular fibrillation threshold (VFT) was measured by electrical stimulation. The expression of connexin43 (CX43) and autophagy-related protein were measured by Western Blot, and correlation analysis was conducted to study the relationship between cardiac autophagy, CX43, and arrhythmia in rats after MI. The effects of WenXin KeLi on arrhythmia, cardiac structure, and function in MI rats were respectively observed by electrical stimulation, cardiac gross section, Masson staining, and cardiac ultrasound. The effects of WenXin KeLi on the expression of phosphoinositide 3 kinase-protein kinase B-mammalian targets of rapamycin (PI3K-AKT-mTOR) autophagy pathway and CX43 were observed by Western Blot.
Results:
After 4 weeks of MI, the VFT in the model group was significantly reduced, the expression levels of yeast ATG6 homolog (Beclin1), microtubule-associated protein 1A/1B-light chain 3 (LC3II/LC3I), and p-CX43 (S368) significantly increased, the expression of sequestosome-1(P62) and CX43 significantly decreased. LC3II/LC3I and Beclin1 expression were significantly negatively correlated with the VFT, and the expression of P62 and CX43 were significantly positively correlated with the VFT. LC3II/LC3I and Beclin1 expression were negatively correlated with CX43 expression, while P62 expression was positively correlated with CX43 expression. WenXin KeLi could significantly increase the VFT, reduce the deposition of collagen fibers, and increase the index levels of the left ventricular end-diastolic anterior wall (LVEDAW), interventricular septum end-diastolic (IVSED), left ventricular end-systolic anterior wall (LVESAW), interventricular septum end-systolic (IVSES), left ventricular end-diastolic posterior wall (LVEDPW), left ventricular end-systolic posterior wall (LVESPW), left ventricular ejection fraction (LVEF) and left ventricular fractional shortening (LVFS), and reduce the index levels of the left ventricular end-diastolic dimension (LVEDD), left ventricular end-systolic dimension (LVESD), left ventricular end-diastolic volume (LVEDV) and left ventricular end-systolic volume (LVESV). WenXin KeLi could increase the expression of CX43, P62, AKT, p-PI3K, p-AKT (308), p-AKT (473), and p-mTOR and decrease the expression of LC3II/LC3I and Beclin1.
Conclusion:
WenXin KeLi can activate the PI3K-AKT-mTOR signaling pathway, improve cardiac autophagy and Cx43 expression in rats after MI, reduce the risk of arrhythmia after MI, and play a cardioprotective role.
More Related Videos
05:41Left Anterior Descending Coronary Artery Ligation for Ischemia-Reperfusion Research: Model Improvement via Technical Modifications and Quality Control
Published on: December 16, 2022
07:40Protection of H9c2 Myocardial Cells from Oxidative Stress by Crocetin via PINK1/Parkin Pathway-Mediated Mitophagy
Published on: May 26, 2023
