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Updated: Jan 8, 2026
A Flow Cytometry-based Assay for Measuring Mitochondrial Membrane Potential in Cardiac Myocytes After Hypoxia/Reoxygenation
Published on: July 13, 2018
Astragaloside IV inhibits MAPK pathway and promotes mitochondrial autophagy in rats with heart failure
Yaoyao Wang1, Yujiang Chen1, Tengxian Li1
1Department of Pathology, The First Affiliated Hospital of Guizhou University of Traditional Chinese Medicine, Guiyang, Guizhou 550000, China.
Abstract:
Heart failure (HF) is a leading cause of morbidity and mortality worldwide, with mitochondrial dysfunction and impaired mitophagy recognized as key contributors to its progression. Astragaloside IV (AS-IV), a major active component of Astragalus membranaceus, has shown multiple biological effects, but its role in mitochondrial homeostasis in HF remains unclear. In this study, a rat model of HF was induced by abdominal aortic constriction, and AS-IV was administered at doses of 20 mg/kg and 80 mg/kg. We found AS-IV treatment significantly reduced myocardial fibrosis and hypertrophy, improved mitochondrial function by increasing ATP and manganese superoxide dismutase levels, reducing reactive oxygen species, and upregulating PGC-1α and TFAM. It also enhanced mitochondrial autophagy. Moreover, AS-IV markedly inhibited the activation of the p38 MAPK pathway. AS-IV suppresses autophagy and mitochondrial function via targeting MAPK pathway in H9c2 cells. These findings suggest that AS-IV alleviates HF by promoting mitophagy and preserving mitochondrial function through suppression of the MAPK pathway, highlighting its potential as a novel therapeutic agent for HF.
Insights
Astragaloside IV (AS-IV) improves heart failure (HF) by enhancing mitochondrial function and mitophagy. This natural compound protects against cardiac damage by suppressing the p38 MAPK pathway.
Area of Science:
- Cardiovascular Biology
- Mitochondrial Medicine
- Pharmacology
Background:
- Heart failure (HF) is a major global health concern linked to mitochondrial dysfunction and impaired mitophagy.
- The therapeutic potential of Astragaloside IV (AS-IV) in HF, particularly regarding mitochondrial homeostasis, is largely unexplored.
Purpose of the Study:
- To investigate the effects of AS-IV on mitochondrial function and mitophagy in a rat model of heart failure.
- To elucidate the underlying molecular mechanisms, including the role of the MAPK pathway.
Main Methods:
- A rat model of heart failure was established using abdominal aortic constriction.
- Rats were treated with AS-IV (20 mg/kg and 80 mg/kg).
- Mitochondrial function, fibrosis, hypertrophy, autophagy, and MAPK pathway activation were assessed.
Main Results:
- AS-IV treatment significantly reduced myocardial fibrosis and hypertrophy.
- Improved mitochondrial function was observed, with increased ATP and manganese superoxide dismutase, reduced reactive oxygen species, and upregulated PGC-1α and TFAM.
- AS-IV enhanced mitochondrial autophagy and inhibited p38 MAPK pathway activation.
Conclusions:
- AS-IV alleviates heart failure by promoting mitophagy and preserving mitochondrial function.
- The therapeutic effects of AS-IV involve the suppression of the MAPK pathway.
- AS-IV shows promise as a novel therapeutic agent for heart failure.
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