Arbutin improves post-myocardial infarction cardiac dysfunction by inhibiting cardiac fibroblast activation.

Background: Arbutin exhibits multiple effects, including anti-inflammatory, antioxidant, and scavenging of free radicals, yet its research within the cardiovascular system remains limited.

Purpose: This study aims to investigate the effects of arbutin on myocardial infarction induced by left anterior descending (LAD) ligation in mice.

Methods: The possible mechanism of arbutin's effect on myocardial infarction was predicted through network pharmacology studies. To evaluate the impact of arbutin on cardiac function in myocardial infarction, TTC staining of the heart was performed, and echocardiography was conducted on mice at different time points. Furthermore, Western blot analysis was utilized not only to detect αSMA, Collagen I, and Collagen III, aiming to investigate the impact of arbutin on myocardial fibrosis but also to detect the influence of arbutin on the phosphorylation level of ERK1/2, thereby elucidating its potential mechanism of action.

Results: Network pharmacology data suggest that arbutin may exert a beneficial effect on myocardial infarction by modulating the ERK1/2 signaling pathway. In vivo experimental results indicate that after myocardial infarction, arbutin can alleviate myocardial fibrosis and cardiac hypertrophy, significantly improving cardiac function. Further in vitro experiments confirm that arbutin markedly reduces fibrosis-related indicators, and this process is partially achieved through the regulation of ERK1/2 phosphorylation.

Conclusion: In conclusion, this study reveals that arbutin exerts a significant protective effect by acting on the ERK1/2 signaling pathway, effectively inhibiting myocardial fibrosis, and subsequently attenuating myocardial infarction induced by LAD ligation.