Bilobalide Prevents Apoptosis and Improves Cardiac Function in Myocardial Infarction

Area of Science:

• Cardiovascular Science
• Pharmacology
• Molecular Biology

Background:

• Myocardial infarction (MI) is a leading cause of global mortality, often resulting in cardiomyocyte apoptosis and myocardial fibrosis.
• Bilobalide (Bilo), a compound from Ginkgo biloba, is known for cardioprotective effects, but its specific role in MI remains unexplored.

Purpose of the Study:

• To investigate the therapeutic effects of Bilobalide (Bilo) on myocardial infarction (MI)-induced cardiac injury.
• To elucidate the underlying molecular mechanisms, particularly the involvement of JNK/p38 MAPK signaling pathways.

Main Methods:

• In vitro studies utilized oxygen-glucose deprivation (OGD)-treated H9c2 cells to assess apoptosis and protein expression.
• In vivo studies involved a myocardial infarction mouse model (left anterior descending artery ligation) to evaluate cardiac function, infarct size, fibrosis, and apoptosis.
• Western blotting and TUNEL staining were employed to analyze signaling pathways and cell apoptosis.

Main Results:

• Bilobalide (Bilo) significantly inhibited OGD-induced apoptosis and LDH release in H9c2 cells, and downregulated p-JNK and p-p38 protein levels.
• In the MI mouse model, Bilo improved cardiac function, reduced infarct size and myocardial fibrosis, and inhibited cardiomyocyte apoptosis.
• Bilo's protective effects were associated with the inactivation of JNK/p38 MAPK signaling pathways.

Conclusions:

• Bilobalide (Bilo) demonstrates significant cardioprotective effects against myocardial infarction (MI)-induced injury, both in vitro and in vivo.
• The mechanism involves the suppression of cardiomyocyte apoptosis and myocardial fibrosis through the inactivation of JNK/p38 MAPK signaling pathways.
• Bilobalide (Bilo) shows promise as an effective therapeutic agent for treating myocardial infarction.