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Taxifolin protects hypoxia-induced cardiomyocytes injury via HIF1-a/HO-1/autophagy pathway 被引量:2
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作者 林骏 谢庆 +5 位作者 赵明一 庄建 陈志衡 蔡骞 叶艳琼 朱平 《South China Journal of Cardiology》 CAS 2017年第2期150-156,共7页
Background Autophagy, a dynamic and efficient process of self-digestion in vivo, has been proven to be ben- eficial for cardiac protection during MI process via removing the additional protein and damaged organelles i... Background Autophagy, a dynamic and efficient process of self-digestion in vivo, has been proven to be ben- eficial 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 de- termination 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 (HIFI-a) and Heine Oxygenase-1 (HO-1) were determined by qRT-PCR. Results Tax at 100μm 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 HIFI-a and HO-1 with Tax. Conclusions Taken together, Tax might be a potential candidate for the treatment of MI by promoting cardio- myocyte autophagy via the activation of HIF 1-a and HO-1. 展开更多
关键词 TAXIFOLIN AUTOPHAGY hifi-a HO-1
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