Cirsiliol alleviates diabetic cardiomyopathy by inhibiting oxidative stress and improving energy metabolism through the PPAR-α/AMPK pathway.

ABSTRACT: Diabetic cardiomyopathy (DCM) is a core cause of heart failure in diabetic patients, with major pathological features including myocardial energy metabolism disorders, mitochondrial dysfunction, oxidative stress, and inflammatory cascades. This study investigates the mechanism by which the flavonoid compound Cirsiliol improves DCM by regulating the peroxisome proliferator-Activated receptor α (PPAR-α)/AMP-activated protein kinase (AMPK) signaling pathway. Using a high-glucose-treated H9C2 myocardial cell model and a streptozotocin-induced diabetic mouse model, the results show that Cirsiliol can dose-dependently increase myocardial cell survival, inhibit high-glucose-induced apoptosis, and significantly improve cardiac function in diabetic mice. Mechanistic studies indicate that Cirsiliol

SUBMITTER: Tao J 

PROVIDER: S-EPMC12816094 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature