Trimetazidine dihydrochloride (Vastarel F) can improve myocardial glucose utilization by inhibiting fatty acid metabolism. Trimetazidine is the first cytoprotective anti-ischemic agent, also used as a vasodilator in ischemic heart disease or angina.

Long-chain 3-ketoacyl thiolase (mitochondrial):75 nM

Trimetazidine up-regulates miR-21 expression, then miR-21 targets PTEN increasing the PI3K pathway and finally the activation of this pathway counteracts the apoptotic effect of hypoxia/reperfusion[3].

The administration of TMZ reduces myocardial infarction size in WT C57BL/6J hearts. Both AMPK and ERK signaling pathways mediate the cardioprotection of TMZ against ischemic injury. Trimetazidine Shifts Metabolism from Fatty Acid Oxidation to Glucose Oxidation and improves Contractile Functions of Cardiomyocytes during Hypoxia[2].

The H9C2 cells are randomly assigned into three groups: Sham group, in which the cells are treated with 0μM TMZ for 48 h and then cultured under normal oxygenation conditions (5% CO2, and 95% air); H/R group, in which cells are treated with 0 μM TMZ for 48 h and then cultured under H/R conditions; and H/R+TMZ group, in which cells are treated with 10 μM TMZ for 48 h and then subjected to H/R treatment. (Only for Reference)