Berberine improved cardiac function and ventricular remodeling in mice after myocardial infarction by inhibiting the macrophage Wnt5a/β-catenin pathway and promoting M2 macrophage differentiation.
Myocardial infarction (MI) is one of the diseases with high fatality rate. Berberine (BBR) is a monomer compound with various biological functions. And some studies have confirmed that BBR plays an important role in alleviating cardiomyocyte injury after MI. However, the specific mechanism is unclear. In this study, we induced a model of MI by ligation of the left anterior descending coronary artery and we surprisingly found that BBR significantly improved ventricular remodeling, with a minor inflammatory and oxidative stress injury, and stronger angiogenesis. Moreover, BBR inhibited the secretion of Wnt5a/β-catenin pathway in macrophages after MI, thus promoting the differentiation of macrophages into M2 type. In summary, BBR effectively improved cardiac function of mice after MI, and the potential protective mechanism was associated with the regulation of inflammatory responses and the inhibition of macrophage Wnt5a/β-catenin pathway in the infarcted heart tissues. Importantly, these findings supported BBR as an effective cardioprotective drug after MI.
Tian et al. (Tue,) conducted a other in Myocardial infarction. Berberine (BBR) was evaluated on Ventricular remodeling, inflammatory and oxidative stress injury, angiogenesis, and macrophage differentiation. Berberine improved cardiac function and ventricular remodeling in mice after myocardial infarction by inhibiting the macrophage Wnt5a/β-catenin pathway and promoting M2 macrophage differentiation.
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