Anemoside B4 improves cardiac function after myocardial infarction by regulating HTR2A/ERK pathway

Area of Science:

• Cardiovascular Research
• Pharmacology
• Molecular Biology

Background:

• Myocardial infarction (MI) remains a leading cause of mortality worldwide.
• Current treatments for MI focus on reperfusion and risk factor management, but often fail to fully restore cardiac function.
• Novel therapeutic strategies targeting cellular protection and inflammation are urgently needed.

Purpose of the Study:

• To investigate the therapeutic role of anemoside B4 (B4) in myocardial infarction (MI).
• To elucidate the underlying molecular mechanisms by which B4 exerts its protective effects in MI.

Main Methods:

• Established rat models of MI and in vitro cardiomyocyte injury.
• Assessed cardiac function, histological changes, apoptosis, and inflammatory markers.
• Utilized network pharmacology and molecular docking to explore the mechanism of action.
• Investigated the role of the HTR2A/ERK pathway in B4's effects.

Main Results:

• Anemoside B4 (B4) significantly improved cardiac function and structure in MI rats.
• B4 reduced cardiomyocyte apoptosis, inflammation, and oxidative stress both in vivo and in vitro.
• B4 demonstrated binding activity with HTR2A, inhibiting HTR2A/ERK pathway activation.
• HTR2A modulation reversed the protective effects of B4, confirming its role in the mechanism.

Conclusions:

• Anemoside B4 (B4) exhibits significant cardioprotective effects against MI.
• The therapeutic benefits of B4 are partly mediated through the inhibition of the HTR2A/ERK signaling pathway.
• B4 represents a promising novel therapeutic candidate for the treatment of myocardial infarction.