Curcumin analogue C66 ameliorates mouse cardiac dysfunction and structural disorders after acute myocardial infarction via suppressing JNK activation

Myocardial infarction contributes to the development of cardiovascular disease, and leads to severe inflamma-tion and health hazards. Our previous studies identified C66, a novel curcumin analogue, had pharmacological benefits in suppressing tissue inflammation. Therefore, the present study hypothesized C66 might improve cardiac function and attenuate structural remodeling after acute myocardial infarction. Administration of 5 mg/ kg C66 for 4-week significantly improved cardiac function and decreased infarct size after myocardial infarction. C66 also effectively reduced cardiac pathological hypertrophy and fibrosis in non-infarct area. In vitro H9C2 cardiomyocytes, C66 also exerted the pharmacological benefits of anti-inflammatory and anti-apoptosis under hypoxic conditions Mechanistically, C66 inhibited cardiac inflammation and cardiomyocyte apoptosis by tar-geting on JNK phosphorylation, whereas replenishment of JNK activation abolished the cardioprotective benefits of C66 treatment. Taken together, curcumin analogue C66 inhibited the activation of JNK signaling, and possessed pharmacological benefits in alleviating myocardial infarction-induced cardiac dysfunction and path-ological tissue injuries.

Automated summary

This study found that the curcumin analogue C66 has protective effects against acute myocardial infarction by inhibiting tissue inflammation and cardiomyocyte apoptosis, improving cardiac function, and reducing infarct size. C66 also alleviates cardiac hypertrophy and fibrosis. The mechanism involves the inhibition of JNK phosphorylation by C66.