Berberine protects cardiac cells against ferroptosis

Area of Science:

• Cardiology
• Cell Biology
• Biochemistry

Background:

• Cardiovascular diseases are a leading cause of mortality, with cardiomyocyte loss being a key feature of cardiac injury.
• Ferroptosis, an iron-dependent cell death characterized by lipid peroxidation, plays a role in conditions like ischemia/reperfusion-induced cardiomyopathy and chemotherapy-induced cardiotoxicity.
• Berberine (BBR) is known to protect the heart from various cardiomyopathies, but its effect on ferroptosis is unexplored.

Purpose of the Study:

• To investigate whether Berberine (BBR) mitigates cardiac cell loss by inhibiting ferroptosis.
• To determine if BBR exhibits protective effects against ferroptosis in cardiac cells.

Main Methods:

• Established a ferroptosis model using erastin and Ras-selective lethal small molecule 3 (RSL3) in H9c2 cardiomyoblast cells and rat neonatal cardiomyocytes.
• Assessed the impact of BBR on cell viability, reactive oxygen species (ROS) accumulation, and lipid peroxidation in the ferroptosis models.
• Quantified Ptgs2 mRNA levels in BBR-treated cells.

Main Results:

• BBR treatment significantly reduced cell viability loss induced by erastin and RSL3 in H9c2 cardiomyoblasts.
• BBR decreased ROS accumulation and lipid peroxidation in cardiac cells undergoing ferroptosis.
• BBR treatment led to reduced Ptgs2 mRNA expression in H9c2 cells and protected rat neonatal cardiomyocytes from RSL3-induced cell death.

Conclusions:

• Berberine (BBR) effectively inhibits ferroptosis in cardiac cells.
• BBR exerts its protective effects by reducing ROS generation and lipid peroxidation.
• These findings suggest BBR as a potential therapeutic agent for conditions involving ferroptosis-mediated cardiac injury.