Protective effect of diminazene attenuates myocardial infarction in rats via increased inflammation and ACE2 activity

Area of Science:

• Cardiology
• Pharmacology
• Biochemistry

Background:

• Myocardial infarction (MI) remains a leading cause of mortality worldwide.
• Understanding the molecular mechanisms underlying MI and identifying effective therapeutic agents are crucial.
• The role of specific signaling pathways, such as the ACE2/AT1R/MasR axis, in MI pathogenesis requires further investigation.

Purpose of the Study:

• To investigate the cardioprotective effects of diminazene in a rat model of acute myocardial infarction (AMI).
• To elucidate the involvement of the angiotensin-converting enzyme 2 (ACE2) signaling pathway in diminazene's therapeutic actions.

Main Methods:

• An acute myocardial infarction (AMI) model was established in rats via left anterior descending coronary artery occlusion.
• AMI rats received intraperitoneal injections of diminazene (5 mg/kg/day) for three days.
• Key protein expressions, inflammatory factors, and infarct size were assessed.

Main Results:

• Diminazene treatment significantly reduced infarct size and inhibited the expression of casein kinase and lactate dehydrogenase in AMI rats.
• Diminazene significantly decreased levels of inflammatory factors (TNF-α, IL-6) and suppressed COX-2 and iNOS protein expression.
• Diminazene activated the expression of ACE2, AT1R, and MasR, indicating activation of the ACE2/AT1R/MasR signaling pathway.

Conclusions:

• Diminazene exhibits significant cardioprotective effects against AMI in a rat model.
• The protective mechanisms involve the suppression of inflammation, reduction of COX-2 and iNOS expression, and activation of the ACE2/AT1R/MasR signaling pathway.
• Diminazene represents a potential therapeutic agent for myocardial infarction, warranting further clinical investigation.