Ginsenoside Rg1 Alleviates Hydrogen Peroxide-Induced Autophagy and Apoptosis in Ovarian Granulosa Cells

Area of Science:

• Reproductive Biology
• Cellular Biology
• Pharmacology

Background:

• Oxidative stress induces apoptosis in ovarian granulosa cells (GCs), leading to premature ovarian failure (POF).
• Ginsenoside Rg1 exhibits antioxidant and anti-apoptotic properties, but its mechanism in ovarian GCs is unclear.
• Understanding Rg1's role in mitochondrial function is crucial for POF treatment.

Purpose of the Study:

• To investigate the mechanism of ginsenoside Rg1 (Rg1) in mitigating oxidative stress, autophagy, and apoptosis in POF.
• To identify key targets and pathways of Rg1 in POF treatment using network pharmacology and in vitro validation.
• To elucidate Rg1's effect on mitochondrial function and the PI3K/AKT/mTOR pathway in H₂O₂-induced POF models.

Main Methods:

• Network pharmacology was used to predict key targets and pathways.
• An in vitro oxidative stress model was established using H₂O₂-treated KGN cells.
• Cell viability, apoptosis rates, reactive oxygen species (ROS), malondialdehyde (MDA), glutathione (GSH), and ATP levels were measured.

Main Results:

• Rg1 treatment significantly improved cell viability and reduced apoptosis in H₂O₂-treated GCs.
• Rg1 suppressed ROS and MDA production while increasing GSH and ATP levels.
• Rg1 downregulated Bax, Caspase-3, Parkin, and PINK1, and upregulated Bcl-2, p-PI3K, p-AKT, and p-mTOR, indicating PI3K/AKT/mTOR pathway activation.

Conclusions:

• Ginsenoside Rg1 protects ovarian GCs against H₂O₂-induced apoptosis.
• Rg1 preserves mitochondrial function and inhibits mitophagy.
• The protective effects of Rg1 involve the regulation of the PI3K/AKT/mTOR signaling pathway.