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Tanshinone IIA Exerts Cardioprotective Effects Through Improving Gut-Brain Axis Post-Myocardial Infarction.
- Source :
-
Cardiovascular toxicology [Cardiovasc Toxicol] 2024 Dec; Vol. 24 (12), pp. 1317-1334. Date of Electronic Publication: 2024 Oct 08. - Publication Year :
- 2024
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Abstract
- Myocardial infarction (MI) is a lethal cardiovascular disease worldwide. Emerging evidence has revealed the critical role of gut dysbiosis and impaired gut-brain axis in the pathological progression of MI. Tanshinone IIA (Tan IIA), a traditional Chinese medicine, has been demonstrated to exert therapeutic effects for MI. However, the effects of Tan IIA on gut-brain communication and its potential mechanisms post-MI are still unclear. In this study, we initially found that Tan IIA significantly reduced myocardial inflammation, apoptosis and fibrosis, therefore alleviating hypertrophy and improving cardiac function following MI, suggesting the cardioprotective effect of Tan IIA against MI. Additionally, we observed that Tan IIA improved the gut microbiota as evidenced by changing the α-diversity and β-diversity, and reduced histopathological impairments by decreasing inflammation and permeability in the intestinal tissues, indicating the substantial improvement of Tan IIA in gut function post-MI. Lastly, Tan IIA notably reduced lipopolysaccharides (LPS) level in serum, inflammation responses in paraventricular nucleus (PVN) and sympathetic hyperexcitability following MI, suggesting that restoration of Tan IIA on MI-induced brain alterations. Collectively, these results indicated that the cardioprotective effects of Tan IIA against MI might be associated with improvement in gut-brain axis, and LPS might be the critical factor linking gut and brain. Mechanically, Tan IIA-induced decreased intestinal damage reduced LPS release into serum, and reduced serum LPS contributes to decreased neuroinflammation with PVN and sympathetic inactivation, therefore protecting the myocardium against MI-induced injury.<br />Competing Interests: Declarations Conflict of interest The authors declare that they have no known competing financial interest or personal relationships that could have appeared to influence the work reported in this paper. Ethical Approval All the animal experiments were approved by Xi’an Jiaotong University Laboratory Animal Administration Committee and were carried out strictly in accordance with Xi’an Jiaotong University Guidelines for Animal Experimentation. Consent to Participate Authors give full consent to participate. Consent for Publication Authors give full consent for publication.<br /> (© 2024. The Author(s).)
- Subjects :
- Animals
Male
Dysbiosis
Anti-Inflammatory Agents pharmacology
Mice, Inbred C57BL
Inflammation Mediators metabolism
Ventricular Function, Left drug effects
Signal Transduction drug effects
Lipopolysaccharides pharmacology
Rats, Sprague-Dawley
Myocardial Infarction physiopathology
Myocardial Infarction pathology
Myocardial Infarction drug therapy
Myocardial Infarction metabolism
Myocardial Infarction prevention & control
Gastrointestinal Microbiome drug effects
Abietanes pharmacology
Disease Models, Animal
Myocardium pathology
Myocardium metabolism
Apoptosis drug effects
Brain-Gut Axis drug effects
Fibrosis
Subjects
Details
- Language :
- English
- ISSN :
- 1559-0259
- Volume :
- 24
- Issue :
- 12
- Database :
- MEDLINE
- Journal :
- Cardiovascular toxicology
- Publication Type :
- Academic Journal
- Accession number :
- 39377990
- Full Text :
- https://doi.org/10.1007/s12012-024-09928-4