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Asiatic Acid Alleviates Myocardial Ischemia-Reperfusion Injury by Inhibiting the ROS-Mediated Mitochondria-Dependent
Chenlong Yi1,2, Meijuan Song3, Lifu Sun2
1Department of Cardiovascular Surgery, The Affiliated Hospital of Yangzhou University, Yangzhou University, Yangzhou, Jiangsu, China.
Abstract:
Myocardial ischemia-reperfusion injury (MIRI) is a major cause of heart failure in patients with coronary heart disease (CHD). Mitochondrial dysfunction is the crucial factor of MIRI; oxidative stress caused by mitochondrial reactive oxygen species (ROS) aggravates myocardial cell damage through the mitochondria-dependent apoptosis pathway. Asiatic acid (AA) is a type of pentacyclic triterpene compound purified from the traditional Chinese medicine Centella asiatica, and its protective pharmacological activities have been reported in various disease models. This study is aimed at investigating the protective effects of AA and the underlying mechanisms in MIRI. To achieve this goal, an animal model of MIRI in vivo and a cell model of oxygen-glucose deprivation/reperfusion (OGD/R) in vitro were established. The results show that AA exerts a protective effect on MIRI by improving cardiac function and reducing cardiomyocyte damage. Due to its antioxidant properties, AA alleviates mitochondrial oxidative stress, as evidenced by the stable mitochondrial structure, maintained mitochondrial membrane potential (MMP), and reduced ROS generation, otherwise due to its antiapoptotic properties. AA inhibits the mitogen-activated protein kinase (MAPK)/mitochondria-dependent apoptosis pathway, as evidenced by the limited phosphorylation of p38-MAPK and JNK-MAPK, balanced proportion of Bcl-2/Bax, reduced cytochrome c release, inhibition of caspase cascade, and reduced apoptosis. In conclusion, our study confirms that AA exerts cardiac-protective effects by regulating ROS-induced oxidative stress via the MAPK/mitochondria-dependent apoptosis pathway; the results provide new evidence that AA may represent a potential treatment for CHD patients.
Insights
Asiatic acid protects the heart from injury by reducing oxidative stress and apoptosis. This compound alleviates damage in myocardial ischemia-reperfusion injury (MIRI) by regulating the MAPK/mitochondria-dependent apoptosis pathway.
Area of Science:
- Cardiovascular Research
- Pharmacology
- Mitochondrial Biology
Background:
- Myocardial ischemia-reperfusion injury (MIRI) is a primary cause of heart failure in coronary heart disease (CHD) patients.
- Mitochondrial dysfunction, particularly oxidative stress from reactive oxygen species (ROS), is central to MIRI-induced cardiomyocyte damage via apoptosis.
- Asiatic acid (AA), derived from *Centella asiatica*, exhibits known protective pharmacological activities.
Purpose of the Study:
- To investigate the cardioprotective effects of Asiatic acid (AA) in myocardial ischemia-reperfusion injury (MIRI).
- To elucidate the underlying mechanisms of AA's protective action in MIRI, focusing on oxidative stress and apoptosis pathways.
Main Methods:
- Established in vivo MIRI animal models and in vitro oxygen-glucose deprivation/reperfusion (OGD/R) cell models.
- Assessed cardiac function, cardiomyocyte damage, mitochondrial structure, mitochondrial membrane potential (MMP), and ROS generation.
- Analyzed the mitogen-activated protein kinase (MAPK) signaling pathway, apoptosis-related proteins (Bcl-2/Bax), cytochrome c release, caspase activity, and apoptosis rates.
Main Results:
- AA significantly improved cardiac function and reduced cardiomyocyte damage in MIRI models.
- AA alleviated mitochondrial oxidative stress by stabilizing mitochondrial structure, maintaining MMP, and decreasing ROS production.
- AA inhibited the MAPK/mitochondria-dependent apoptosis pathway, evidenced by reduced p38-MAPK and JNK-MAPK phosphorylation, balanced Bcl-2/Bax ratio, decreased cytochrome c release, and suppressed caspase activation, ultimately reducing apoptosis.
Conclusions:
- Asiatic acid demonstrates significant cardioprotective effects against MIRI.
- AA functions by mitigating ROS-induced oxidative stress and inhibiting the MAPK/mitochondria-dependent apoptosis pathway.
- These findings suggest AA holds potential as a therapeutic agent for patients with coronary heart disease experiencing MIRI.
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