Sesamin prevents apoptosis and inflammation after experimental myocardial infarction by JNK and NF-κB pathways

Area of Science:

• Cardiology
• Pharmacology
• Molecular Biology

Background:

• Myocardial infarction (MI) can lead to severe cardiac dysfunction, often exacerbated by inflammatory responses and left ventricular remodeling.
• Understanding the molecular mechanisms behind post-MI cardiac remodeling is crucial for developing effective therapeutic strategies.

Purpose of the Study:

• To investigate the cardioprotective effects of sesamin in a mouse model of myocardial infarction.
• To elucidate the underlying mechanisms, focusing on sesamin's impact on apoptosis, inflammation, and the JNK/NF-κB signaling pathways.

Main Methods:

• Myocardial infarction was induced in mice via left anterior descending coronary artery ligation.
• Mice were treated with sesamin via gavage for one week post-MI.
• Histopathological examination, apoptosis factor analysis, cytokine expression, and Western blotting for JNK and NF-κB signaling were performed.

Main Results:

• Sesamin treatment significantly alleviated cardiac damage and reduced myocardial apoptosis in the border zone of the infarcted heart.
• Sesamin mitigated the inflammatory response by decreasing cytokine expression and inactivating the NF-κB signaling pathway.
• Sesamin reduced p-JNK protein levels, restoring the balance of Bcl-2 and Bax proteins, thereby inhibiting pro-apoptotic signaling.

Conclusions:

• Sesamin demonstrates significant cardioprotective effects against myocardial infarction in a mouse model.
• The cardioprotection is attributed to sesamin's ability to decrease myocardial apoptosis and suppress inflammatory responses.
• Sesamin may represent a potential therapeutic agent for managing cardiac dysfunction post-MI by modulating JNK and NF-κB pathways.