We established myocardial injury models in vivo and in vitro to investigate the cardioprotective effect of gomisin D obtained from Schisandra chinensis . Gomisin D significantly inhibited isoproterenol-induced apoptosis and hypertrophy in H9C2 cells. Gomisin D decreased serum BNP, ANP, CK-MB, cTn-T levels and histopathological alterations, and inhibited myocardial hypertrophy in mice. In mechanisms research, gomisin D reversed ISO-induced accumulation of intracellular ROS and Ca 2+ . Gomisin D further improved mitochondrial energy metabolism disorders by regulating the TCA cycle. These results demonstrated that gomisin D had a significant effect on isoproterenol-induced myocardial injury by inhibiting oxidative stress, calcium overload and improving mitochondrial energy metabolism.
Keyphrases
- induced apoptosis
- oxidative stress
- diabetic rats
- endoplasmic reticulum stress
- signaling pathway
- high glucose
- dna damage
- ischemia reperfusion injury
- drug induced
- high fat diet induced
- cell proliferation
- protein kinase
- endothelial cells
- heart failure
- type diabetes
- skeletal muscle
- adipose tissue
- heat stress
- heat shock
- insulin resistance