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首页> 外文期刊>American Journal of Physiology >Reactive oxygen species production by mitochondria in endothelial cells exposed to reoxygenation after hypoxia and glucose depletion is mediated by ceramide.
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Reactive oxygen species production by mitochondria in endothelial cells exposed to reoxygenation after hypoxia and glucose depletion is mediated by ceramide.

机译：低氧和葡萄糖耗竭后暴露于复氧的内皮细胞中线粒体产生的活性氧由神经酰胺介导。

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摘要

In endothelium, reoxygenation after hypoxia (H/R) has been shown to induce production of reactive oxygen species (ROS) by complex III of the mitochondrial respiratory chain. The purpose of the present study was to test the involvement of ceramide in this phenomenon. Human umbilical vein endothelial cells underwent 2 h of hypoxia (PO2, approximately 20 mmHg) without glucose and 1 h of reoxygenation (PO2, approximately 120 mmHg) with glucose. ROS production was measured by the fluorescent marker 2',7'-dichlorodihydrofluorescein diacetate, and cell death by propidium iodide. We showed that 1) after 1 h of reoxygenation, fluorescence had risen and that ROS production was inhibited by desipramine, an inhibitor of sphingomyelinase, an enzyme responsible for ceramide production (126 +/- 7% vs. 48 +/- 12%, P < 0.05); 2) administration of ceramide (N-acetylsphingosine) per se (i.e., in the absence of H/R) induced ROS production (65 +/- 3%), which was inhibited by complex III inhibitor: antimycin A (24 +/- 3%, P< 0.0001), or stigmatellin (31 +/- 2%, P < 0.0001); 3) hypoxia/reoxygenation-induced ROS production was not affected by either ceramide-activated protein kinase inhibitor dimethyl aminopurine or mitochondrial permeability transition inhibitor cyclosporin A but was significantly inhibited by the antiapoptotic protein Bcl-2 (82 +/- 8%, P < 0.05); 4) ceramide-induced ROS production was also inhibited by Bcl-2 (41 +/- 4%, P < 0.0001). These results demonstrate that in endothelial cells submitted to hypoxia and glucose depletion followed by reoxygenation with glucose, the pathway implicated in mitochondrial complex III ROS production is ceramide dependent and is decreased by the antiapoptotic protein Bcl-2.
机译：在内皮中，低氧后的复氧（H / R）已显示可通过线粒体呼吸链复合物III诱导产生活性氧（ROS）。本研究的目的是测试神经酰胺在这种现象中的参与。人脐静脉内皮细胞在没有葡萄糖的情况下经历了2小时的缺氧（PO2，大约20 mmHg），在经历了葡萄糖的情况下进行了1 h的复氧（PO2，大约120 mmHg）。用荧光标记2'，7'-二氯二氢荧光素二乙酸酯测量ROS的产生，用碘化丙啶测量细胞死亡。我们发现1）复氧1小时后，荧光增强，ROS的产生被神经鞘磷脂酶的一种抑制剂神经鞘氨醇抑制，desipramine是神经酰胺产生的一种酶（126 +/- 7％对48 +/- 12％， P <0.05）; 2）本身（即在没有H / R的情况下）施用神经酰胺（N-乙酰基鞘氨醇）可诱导ROS产生（65 +/- 3％），其被复合物III抑制剂：抗霉素A（24 +/-）抑制3％，P <0.0001）或柱头蛋白（31 +/- 2％，P <0.0001）; 3）低氧/复氧诱导的ROS的产生不受神经酰胺激活的蛋白激酶抑制剂二甲基氨基嘌呤或线粒体通透性过渡抑制剂环孢菌素A的影响，但被抗凋亡蛋白Bcl-2显着抑制（82 +/- 8％，P < 0.05）; 4）Bcl-2也抑制了神经酰胺诱导的ROS的产生（41 +/- 4％，P <0.0001）。这些结果表明，在经历缺氧和葡萄糖耗竭然后再用葡萄糖复氧的内皮细胞中，与线粒体复合物III ROS产生有关的途径是神经酰胺依赖性的，并且被抗凋亡蛋白Bcl-2减少。

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