Ginsenoside Rg1 treats chronic heart failure by downregulating ERK1/2 protein phosphorylation

Area of Science:

• Cardiovascular Research
• Pharmacology
• Molecular Biology

Background:

• Chronic heart failure (CHF) is a complex condition with high morbidity and mortality.
• Current treatments for CHF have limitations, necessitating the exploration of novel therapeutic agents.
• Ginsenoside Rg1 (GRg1), a natural compound, has shown potential in preclinical studies for various conditions.

Purpose of the Study:

• To investigate the therapeutic mechanism of ginsenoside Rg1 (GRg1) in chronic heart failure (CHF).
• To examine the effect of GRg1 on ERK1/2 protein phosphorylation in the context of CHF.
• To evaluate the protective effects of GRg1 on cardiac cells and function in experimental models of CHF.

Main Methods:

• Utilized H9c2 cardiomyocytes and an in vivo adriamycin (ADR)-induced CHF rat model.
• Groups included control, CHF (ADR), and CHF+ginsenoside Rg1.
• Assessed cell viability, proliferation, apoptosis, and protein expression (ERK1/2, Bcl-2, Caspase3, Bax).
• Measured serum NT-proBNP levels, heart weight/body weight index, and performed electrocardiogram analysis.

Main Results:

• GRg1 treatment enhanced cell viability and proliferation in H9c2 cells.
• GRg1 significantly reduced apoptosis and inflammatory factors in both cellular and in vivo models.
• GRg1 upregulated Bcl-2 expression and downregulated Caspase3 and Bax expression.
• GRg1 administration decreased serum NT-proBNP, reduced the HW/BW index, and improved electrocardiogram parameters in CHF rats.
• GRg1 inhibited ERK1/2 protein phosphorylation in the CHF model.

Conclusions:

• Ginsenoside Rg1 (GRg1) demonstrates significant therapeutic potential for chronic heart failure (CHF).
• GRg1 alleviates CHF by inhibiting ERK1/2 protein phosphorylation, thereby reducing apoptosis and inflammation.
• GRg1 enhances cardiac cell activity and proliferation, offering a promising natural therapeutic agent for CHF.