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首页> 外文期刊>Biochimica et biophysica acta. Molecular basis of disease: BBA >Mangiferin protects mitochondrial function by preserving mitochondrial hexokinase-II in vessel endothelial cells
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Mangiferin protects mitochondrial function by preserving mitochondrial hexokinase-II in vessel endothelial cells

机译:Mangiferin通过在血管内皮细胞中保留线粒体六酮酶-II来保护线粒体功能

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摘要

Hexokinase-II (HK-II) confers protection against cell death and this study was designed to investigate the effect of mangiferin on the regulation of mitochondrial HK-II. In vessel endothelial cells, saturated fatty acid palmitate (PA) stimulation induced HK-II detachment from mitochondria due to cellular acidification. Mangiferin reduced lactate accumulation by improving pyruvate dehydrogenase activity, promoted Akt translocation to and prevented HK-II detachment from mitochondria. Knockdown of Akt2 diminished the protective effect of mangiferin on mitochondrial HK-II, confirming the role of Akt in the regulation of HK-II. Mangiferin prevented mitochondrial permeability transition pore opening, restored mitochondrial membrane potential and thereby protected cell from apoptosis. In high-fat diet fed mice, oral administration of mangiferin induced Akt phosphorylation, increased HK-II binding to mitochondria and resultantly protected vessel endothelial function, demonstrating its protective effect on endothelial integrity in vivo. This finding provided a novel strategy for the protection of mitochondrial function in the endothelium.
机译:六酮酶-II(HK-II)赋予对细胞死亡的保护,旨在探讨Mangiferin对线粒体HK-II调控的影响。在血管内皮细胞中,由于细胞酸化,饱和脂肪酸棕榈酸盐(PA)刺激诱导线粒体的HK-II脱离。 Mangiferin通过改善丙酮酸脱氢酶活性降低乳酸乳酸积累,促进Akt易位和预防线粒体的HK-II脱离。 AKT2的敲低减少了Mangiferin对线粒体HK-II的保护作用,证实AKT在HK-II的调节中的作用。 Mangiferin防止线粒体渗透率过渡孔开口,恢复的线粒体膜电位,从而受到凋亡的保护细胞。在高脂饮食喂养小鼠中,人口素诱导磷酸化的口服施用,增加了对线粒体的HK-II结合,并产生了保护的血管内皮功能,证明了其对体内内皮完整性的保护作用。该发现提供了一种用于保护内皮中线粒体功能的新策略。

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