Ginsenoside Rb1 Inhibits Cardiomyocyte Autophagy via PI3K/Akt/mTOR Signaling Pathway and Reduces Myocardial...

Area of Science:

• Cardiovascular Research
• Pharmacology
• Cellular Biology

Background:

• Myocardial ischemia/reperfusion injury (MIRI) is a significant cause of heart damage during acute myocardial infarction, posing a clinical challenge.
• Ginsenoside Rb1 demonstrates cardiovascular protective effects, but its underlying mechanism in MIRI is not fully understood.

Purpose of the Study:

• To investigate the protective mechanisms of Ginsenoside Rb1 against MIRI in both in vivo and in vitro models.
• To elucidate the role of autophagy and the PI3K/Akt/mTOR pathway in Ginsenoside Rb1's cardioprotective effects.

Main Methods:

• Evaluated infarct size using TTC staining in a rat MIRI model.
• Assessed cell apoptosis via TUNEL assay and flow cytometry.
• Analyzed apoptosis, autophagy, and PI3K/Akt/mTOR pathway proteins using Western blot and immunohistochemistry.
• Measured inflammatory cytokine levels (IL-1β, TNF-α, IL-6) with ELISA.

Main Results:

• Ginsenoside Rb1 treatment reduced MIRI in rats and protected H9C2 cells from hypoxia/reoxygenation injury.
• Ginsenoside Rb1 inhibited MIRI-induced autophagy activation; autophagy inhibition enhanced its protective effects.
• Ginsenoside Rb1 activated the PI3K/Akt/mTOR pathway, which was crucial for its protective actions.

Conclusions:

• Ginsenoside Rb1 protects against MIRI by suppressing cardiomyocyte autophagy through the PI3K/Akt/mTOR signaling pathway.
• This study reveals a novel mechanism for Ginsenoside Rb1's cardioprotective effects, offering potential therapeutic insights.