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首页> 外文期刊>The Journal of Nutritional Biochemistry >Apoptosis induced by oxidized lipids is associated with up-regulation of p66Shc in intestinal Caco-2 cells: protective effects of phenolic compounds.
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Apoptosis induced by oxidized lipids is associated with up-regulation of p66Shc in intestinal Caco-2 cells: protective effects of phenolic compounds.

机译：氧化脂质诱导的凋亡与肠Caco-2细胞中p66Shc的上调相关：酚类化合物的保护作用。

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In this study, we investigated the alterations of the redox balance induced by the lipid fraction of oxLDL in Caco-2 intestinal cells, and the effects of tyrosol and protocatechuic acid, two dietary phenolic compounds. We found that oxidized lipids extracted from oxLDL (LipE) induced oxidative stress by determining, 6 h after treatment, ROS overproduction (about a 100% and a 43% increase of O2- and H2O2 production, respectively, P<.05: LipE vs. control) and, 12 h after treatment, GSH depletion (about a 26% decrease, P<.05: LipE vs. control), and by impairing the activities of superoxide dismutase, catalase and glutathione peroxidase. In response to the induced oxidative stress, we observed significant overexpression of glutathione peroxidase (6 h after treatment: P<.05), glutathione reductase and gamma-glutamylcysteine synthetase (12 h after treatment: P<.05). Notably, when GSH depletion occurred, p66Shc protein expression increased by about 300% with respect to control (P<.001; LipE vs. control). These effects were fully counteracted by dietary phenolics which inhibited ROS overproduction and GSH consumption, rendered the reactive transcription of glutathione-associated enzymes unnecessary and blocked the intracellular signals leading to the overexpression and rearrangement of p66Shc signalling molecule. Altogether, these results suggest that the impairment of the antioxidant system hijacks intestinal cells towards an apoptotic-prone phenotype via the activation of p66Shc molecule. They also propose a reappraisal of dietary polyphenols as intestinal protecting agents, indicating the antiapoptotic effect as a further mechanism of action of these antioxidant compounds. All rights reserved, Elsevier.
机译：在这项研究中，我们调查了oxLDL脂质部分在Caco-2肠道细胞中诱导的氧化还原平衡的变化，以及两种饮食酚类化合物酪醇和原儿茶酸的影响。我们发现通过从oxLDL（LipE）中提取的氧化脂质通过确定处理后6小时ROS过量生产（分别将O2和H2O2的产量分别增加100％和43％，P <.05：LipE vs对照）和治疗后12小时，GSH耗竭（减少约26％，P <0.05：LipE与对照相比），并且损害了超氧化物歧化酶，过氧化氢酶和谷胱甘肽过氧化物酶的活性。响应诱导的氧化应激，我们观察到谷胱甘肽过氧化物酶（处理后6小时：P <.05），谷胱甘肽还原酶和γ-谷氨酰半胱氨酸合成酶（处理后12小时：P <.05）明显过表达。值得注意的是，当发生GSH耗竭时，相对于对照，p66Shc蛋白表达增加了约300％（P <.001; LipE与对照相比）。这些作用被饮食中的酚类物质完全抵消，后者抑制了ROS的过度产生和GSH的消耗，使谷胱甘肽相关酶的反应性转录变得不必要，并阻止了导致p66Shc信号分子过度表达和重排的细胞内信号。总而言之，这些结果表明抗氧化系统的损伤通过激活p66Shc分子将肠道细胞劫持成易于凋亡的表型。他们还提议对膳食多酚作为肠道保护剂进行重新评估，表明抗凋亡作用是这些抗氧化剂化合物的进一步作用机理。保留所有权利，Elsevier。

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