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Arbutin improves post-myocardial infarction cardiac dysfunction by inhibiting cardiac fibroblast activation
Yun Liu1, Xuemei Liu2, Xuan Zhang1
1Department of Emergency Medicine, Qilu Hospital of Shandong University, Jinan 250012, China; Shandong Provincial Clinical Research Center for Emergency and Critical Care Medicine, Institute of Emergency and Critical Care Medicine of Shandong University, Chest Pain Center, Qilu Hospital of Shandong University, Jinan, China; Medical and Pharmaceutical Basic Research Innovation Center of Emergency and Critical Care Medicine, China's Ministry of Education, Shandong Provincial Engineering Laboratory for Emergency and Critical Care Medicine, Key Laboratory of Emergency and Critical Care Medicine of Shandong Province, Key Laboratory of Cardiopulmonary-Cerebral Resuscitation Research of Shandong Province, Qilu Hospital of Shandong University, Jinan, China; NMPA Key Laboratory for Clinical Research and Evaluation of Innovative Drug, Qilu Hospital of Shandong University, Jinan, China; National Key Laboratory for Innovation and Transformation of Luobing Theory, The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences, Qilu Hospital of Shandong University, Jinan, China.
Insights
Arbutin protects against myocardial infarction by reducing cardiac fibrosis and improving heart function. This study highlights arbutin
Area of Science:
- Cardiovascular Research
- Pharmacology
- Biomedical Science
Background:
- Arbutin possesses anti-inflammatory, antioxidant, and free radical scavenging properties.
- Research on arbutin's cardiovascular effects is limited.
Purpose of the Study:
- To investigate the cardioprotective effects of arbutin in a mouse model of myocardial infarction.
- To elucidate the underlying mechanisms of arbutin's action.
Main Methods:
- Network pharmacology was used to predict potential mechanisms.
- Myocardial infarction was induced by left anterior descending (LAD) ligation in mice.
- Cardiac function was assessed using TTC staining and echocardiography.
- Western blot analysis was employed to evaluate myocardial fibrosis and ERK1/2 signaling pathway activation.
Main Results:
- Network pharmacology suggested arbutin modulates the ERK1/2 pathway.
- Arbutin treatment attenuated myocardial fibrosis and cardiac hypertrophy post-myocardial infarction.
- Arbutin significantly improved cardiac function and reduced fibrosis markers, partly via ERK1/2 regulation.
Conclusions:
- Arbutin demonstrates significant cardioprotective effects against myocardial infarction.
- The protective mechanism involves the ERK1/2 signaling pathway, inhibiting myocardial fibrosis.
- Arbutin holds potential for treating myocardial infarction-induced cardiac damage.
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.
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