Taxifolin protects hypoxia-induced cardiomyocytes injury via HIF1-a/HO-1/autophagy pathway

Background Autophagy, a dynamic and efficient process of self-digestion in vivo, has been proven to be beneficial for cardiac protection during MI process via removing the additional protein and damaged organelles in the heart. Taxifolin(Tax), a common plant flavonoid, has been widely used for the treatment of myocardial infarction. However, the underlying mechanism of Tax is largely unknown. Methods Murine arterial cardiomyocytes HL-1 cells were pretreated with Tax and then exposed to hypoxia environment. CCK-8 was performed for the determination of cell viability. Monodansylcadaverine(MDC) and Microtubule-associated protein 1A/1B-light chain3(LC3) were analyzed by immunofluorescence staining. The relative gene expressions of Hypoxia Inducible Factor-1(HIF1-a) and Heme Oxygenase-1(HO-1) were determined by qRT-PCR. Results Tax at 100 μm for 6 h has the maximal effect to avoid reducing the cell viability excessively and significantly abolished hypoxia-induced cell death. Both of the MDC and LC3 immunofluorescence staining revealed markedly increase of expression of autophagy with pretreatment of Tax. Finally, qRT-PCR showed the upregulation of HIF1-a and HO-1 with Tax.Conclusions Taken together, Tax might be a potential candidate for the treatment of MI by promoting cardiomyocyte autophagy via the activation of HIF1-a and HO-1.