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首页> 外文期刊>Drug Design, Development and Therapy >The neuroprotective effects of curcumin are associated with the regulation of the reciprocal function between autophagy and HIF-1α in cerebral ischemia-reperfusion injury
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The neuroprotective effects of curcumin are associated with the regulation of the reciprocal function between autophagy and HIF-1α in cerebral ischemia-reperfusion injury

机译：姜黄素的神经保护作用与自噬与HIF-1α在脑缺血再灌注损伤中的相互调节有关

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Purpose: The beneficial, neuroprotective effects of curcumin against ischemia-reperfusion injury have been demonstrated. In the present study, whether curcumin exerts neuroprotective effects associated with the inhibition of autophagy and hypoxia inducible factor-1α (HIF-1α) was investigated. Materials and methods: PC12 cellular model of oxygen glucose deprivation/reperfusion (OGD/R) has been developed to mimic cerebral ischemia-reperfusion injury. Cell viability was evaluated using the CellTiter 96sup?/sup AQsubueous/sub One Solution Cell Proliferation Assay. Apoptosis was assessed using flow cytometry. The expression levels of HIF-1α and autophagy-associated proteins, LC3 and P62, were examined using Western blot. The autophagy flux was quantitatively estimated based on the number of autophagic compartments using fluorescence microscopy. In addition, 3-methyladenine (3-MA) was administered to PC12 cells to investigate how autophagy affects HIF-1α. Moreover, the inhibitory effects of HIF-1α on autophagy activation level were examined. Results: In this study, curcumin decreased the death and apoptosis of cells, and inhibited autophagy and HIF-1α under OGD/R conditions, consistent with 3-MA treatment or HIF-1α downregulation. Moreover, inhibition of autophagy caused a decrease in HIF-1α, and the attenuation of HIF-1α induced autophagy suppression under OGD/R conditions. Conclusion: The results of this study showed that curcumin exerts neuroprotective effects against ischemia-reperfusion, which is associated with the regulation of the reciprocal function between autophagy and HIF-1α.
机译：目的：姜黄素对缺血再灌注损伤具有有益的神经保护作用。在本研究中，研究姜黄素是否发挥与自噬和缺氧诱导因子-1α（HIF-1α）抑制相关的神经保护作用。材料和方法：已经开发了PC12氧葡萄糖剥夺/再灌注（OGD / R）细胞模型来模拟脑缺血-再灌注损伤。使用CellTiter 96 ？ AQ ueus One Solution细胞增殖测定法评估细胞活力。使用流式细胞仪评估细胞凋亡。使用蛋白质印迹法检测HIF-1α和自噬相关蛋白LC3和P62的表达水平。使用荧光显微镜，根据自噬区室的数量定量估计自噬通量。此外，还对PC12细胞施用了3-甲基腺嘌呤（3-MA），以研究自噬如何影响HIF-1α。此外，检查了HIF-1α对自噬激活水平的抑制作用。结果：在这项研究中，姜黄素可降低细胞的死亡和凋亡，并在OGD / R条件下抑制自噬和HIF-1α，这与3-MA治疗或HIF-1α的下调一致。此外，在OGD / R条件下，自噬的抑制导致HIF-1α的降低，而HIF-1α的减弱导致自噬的抑制。结论：这项研究的结果表明姜黄素对缺血再灌注具有神经保护作用，这与自噬和HIF-1α之间的相互调节有关。

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