Dihydroartemisinin ameliorates palmitate-induced apoptosis in cardiomyocytes via regulation on miR-133b/Sirt1 axis

Excessive fat ectopically deposited in the non-adipose tissues is considered as one of the leading causes of myopathy. The aim of this study was to investigate the role of Dihydroartemisinin (DHA) in palmitate (PAL)incubated H9c2 cells (lipotoxicity-induced cell injury model). Cell viability of PAL-treated cells was determined by MTT assay, and apoptotic regulators were examined by qRT-PCR and western blot analysis, in the absence or in the presence of DHA, respectively. Expression levels of miR-133b and Sirt1 were also evaluated by qRT-PCR and western blotting examination. PAL decreased the viability of H9c2 cells and enhanced the expression of apoptotic genes. DHA reversed the effect of PAL on cell viability and lowed the level of Caspase3 and Bax. It also lowered the expression of miR-133b, while enhanced the expression of Bcl-2. Sirt1 was revealed as target of miR-133b through transcriptional regulation and the process was affected by DHA. DHA partially protected against the PAL-induced lipotoxicity by influencing the expression of miR-133b that hindered the activity of Sirt1. DHA may be used as a potential treatment in clinical management for lipotoxicity induced heart complications.