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

LIN Jun; XIE Qing; ZHAO Ming-yi; ZHUANG Jian; CHEN Zhi-heng; CAI Qian; YE Yan-qiong; ZHU Ping

摘要：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 chain 3 (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.