Luteolin alleviates post-infarction cardiac dysfunction by up-regulating autophagy through Mst1 inhibition.

ABSTRACT: Myocardial infarction (MI), which is characterized by chamber dilation and LV dysfunction, is associated with substantially higher mortality. We investigated the effects and underlying mechanisms of Luteolin on post-infarction cardiac dysfunction. Myocardial infarction was constructed by left anterior descending coronary artery ligation. In vitro, cultured neonatal cardiomyocytes subjected to simulated MI were used to probe mechanism. Luteolin significantly improved cardiac function, decreased cardiac enzyme and inflammatory cytokines release after MI. Enhanced autophagic flux as indicated by more autophagosomes puncta, less accumulation of aggresomes and P62 in the neonatal cardiomyocytes after hypoxia was observed in the Luteolin pre-treatment group. Western blot analysis also demonstrat

SUBMITTER: Hu J 

PROVIDER: S-EPMC4717847 | biostudies-literature | 2016 Jan

REPOSITORIES: biostudies-literature