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Published on: January 10, 2025
Berberine Intervention Mitigates Myocardial Ischemia-Reperfusion Injury in a Rat Model: Mechanistic Insights via
Haichen Yang1, Gang Cao2, Xia Li3
1Department of Emergency, The Affiliated Huai'an Hospital of Xuzhou Medical University and Huai'an second People's Hospital, Huai'an, People's Republic of China.
Background:
Ischemia-reperfusion (I/R) injury is a major contributor to myocardial dysfunction and tissue damage. A natural alkaloid-Berberine having a wide range of pharmacological properties, has garnered interest for its potential cardioprotective properties. This study aimed to investigate the protective effects of berberine on myocardial tissue in a rat model of myocardial ischemia-reperfusion (I/R) injury. Additionally, the study explored the role of the miR-184/NOTCH1 signaling pathway in mediating these effects.
Methods:
Male Wistar rats were randomly assigned to five groups: sham-operated control, I/R injury, I/R treated with berberine, I/R treated with inhibitor NC and I/R treated with a miR-184 inhibitor. The I/R injury was induced by ligating the left anterior descending (LAD) coronary artery for 30 minutes, followed by 2 hours of reperfusion. Berberine was administered orally at 100 mg/kg/day for 2 weeks, and the miR-184 inhibitor was administered via intraperitoneal injection. Hemodynamic parameters were recorded using a pressure sensor connected to a catheter inserted into the left ventricle. Myocardial infarct size was assessed using TTC staining, while histological and molecular changes were evaluated through H&E staining, TUNEL assay, and Western blotting. The expression levels of target genes were analyzed using quantitative real-time PCR (qRT-PCR).
Results:
Berberine significantly reduced myocardial infarct size and improved hemodynamic parameters compared to the untreated I/R group. Additionally, berberine treatment attenuated apoptosis as evidenced by decreased TUNEL-positive cells. The miR-184 inhibitor also demonstrated protective effects by modulating key signaling pathways involved in myocardial injury. Western blot analysis revealed downregulation of NOTCH1 and HES1 expression in treated groups, indicating a potential mechanism for the observed cardio protection.
Conclusion:
Berberine and miR-184 inhibition offer significant protection against myocardial ischemia-reperfusion injury. These findings suggest that targeting miR-184 and associated pathways may be a promising therapeutic strategy for reducing cardiac damage following ischemia-reperfusion.
