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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Deletion of the p66Shc longevity gene reduces systemic and tissue oxidative stress, vascular cell apoptosis, and early atherogenesis in mice fed a high-fat diet.
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Deletion of the p66Shc longevity gene reduces systemic and tissue oxidative stress, vascular cell apoptosis, and early atherogenesis in mice fed a high-fat diet.

机译：p66Shc长寿基因的删除减少了高脂饮食小鼠的全身和组织氧化应激，血管细胞凋亡和早期动脉粥样硬化。

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摘要

Several experimental and clinical studies have shown that oxidized low-density lipoprotein and oxidation-sensitive mechanisms are central in the pathogenesis of vascular dysfunction and atherogenesis. Here, we have used p66(Shc-/-) and WT mice to investigate the effects of high-fat diet on both systemic and tissue oxidative stress and the development of early vascular lesions. To date, the p66(Shc-/-) mouse is the unique genetic model of increased resistance to oxidative stress and prolonged life span in mammals. Computer-assisted image analysis revealed that chronic 21% high-fat treatment increased the aortic cumulative early lesion area by approximately 21% in WT mice and only by 3% in p66(Shc-/-) mice. Early lesions from p66(Shc-/-) mice had less content of macrophage-derived foam cells and apoptotic vascular cells, in comparison to the WT. Furthermore, in p66(Shc-/-) mice, but not WT mice, we found a significant reduction of systemic and tissue oxidative stress (assessed by isoprostanes, plasma low-density lipoprotein oxidizability, and the formation of arterial oxidation-specific epitopes). These results support the concept that p66(Shc-/-) may play a pivotal role in controlling systemic oxidative stress and vascular diseases. Therefore, p66(Shc) might represent a molecular target for therapies against vascular diseases.
机译：几项实验和临床研究表明，氧化型低密度脂蛋白和氧化敏感性机制在血管功能障碍和动脉粥样硬化的发病机理中至关重要。在这里，我们已经使用p66（Shc-/-）和WT小鼠来研究高脂饮食对全身和组织氧化应激以及早期血管病变的发展的影响。迄今为止，p66（Shc-/-）小鼠是提高哺乳动物对氧化应激的抵抗力和延长寿命的独特遗传模型。计算机辅助图像分析显示，慢性21％高脂治疗在WT小鼠中使主动脉累积早期病变面积增加约21％，而在p66（Shc-/-）小鼠中仅增加3％。与WT相比，p66（Shc-/-）小鼠的早期病变具有较少的巨噬细胞源性泡沫细胞和凋亡性血管细胞。此外，在p66（Shc-/-）小鼠而非WT小鼠中，我们发现全身和组织氧化应激显着降低（通过异前列腺素，血浆低密度脂蛋白氧化性和动脉氧化特异性表位的形成进行评估） 。这些结果支持p66（Shc-/-）可能在控制系统性氧化应激和血管疾病中起关键作用的概念。因此，p66（Shc）可能代表血管疾病治疗的分子靶标。

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