平滑肌细胞的迁移是形成AS的重要原因,而氧化应激是VSMC增殖和迁移的主要因素之一。除了黄嘌呤氧化酶,环氧化酶和脂氧化酶,未偶联的内皮一氧化的英语翻译

平滑肌细胞的迁移是形成AS的重要原因,而氧化应激是VSMC增殖和迁移的

平滑肌细胞的迁移是形成AS的重要原因,而氧化应激是VSMC增殖和迁移的主要因素之一。除了黄嘌呤氧化酶,环氧化酶和脂氧化酶,未偶联的内皮一氧化氮合酶,过氧化物酶和NADPH氧化酶103,线粒体酶也是细胞产生ROS的主要酶104、105。线粒体解偶联蛋白(UCPs)是线粒体内膜中的蛋白质,属于线粒体阴离子转运蛋白的超家族,通过控制质子穿过线粒体内膜的泄漏,使ATP合成与氧化磷酸化脱钩。因而可以通过维持ROS稳态来减少氧化应激并防止氧化损伤106。在UCP的成员中,UCP2被认为对防止氧化应激很重要108。大量研究报道,增加的UCP2表达可减轻氧化剂组织的损伤109。而且,激活PPARγ抵抗衰老的脑动脉中的氧化损伤与上调UCP2110有关。
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The migration of smooth muscle cells is an important reason for the formation of AS, and oxidative stress is one of the main factors for the proliferation and migration of VSMC. In addition to xanthine oxidase, cyclooxygenase and lipoxygenase, uncoupled endothelial nitric oxide synthase, peroxidase and NADPH oxidase 103, mitochondrial enzymes are also the main enzymes 104, 105 that produce ROS in cells. Mitochondrial uncoupling proteins (UCPs) are proteins in the inner mitochondrial membrane and belong to the superfamily of mitochondrial anion transporters. They decouple ATP synthesis from oxidative phosphorylation by controlling the leakage of protons through the inner mitochondrial membrane. Therefore, it is possible to reduce oxidative stress and prevent oxidative damage 106 by maintaining ROS homeostasis. Among UCP members, UCP2 is considered to be important for preventing oxidative stress108. A large number of studies have reported that increased UCP2 expression can reduce the damage of oxidant tissues109. Moreover, activating PPARγ to resist oxidative damage in aging cerebral arteries is related to up-regulation of UCP2110.
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结果 (英语) 2:[复制]
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The migration of smooth muscle cells is an important reason for the formation of AS, and oxidative stress is one of the main factors of VSMC proliferation and migration. In addition to jaundice oxidase, cyclooxidase and lipid oxidase, unassumed endotrophic nitric oxide enzyme, peroxidase and NADPH oxidase 103, mitochondrase is also the main enzyme in cells producing ROS 104, 105. Mitochondrial decoupling protein (UCPs) is a protein in the membrane of mitochondrial body, belonging to the super-family of mitochondrial anion transport protein, by controlling the leakage of protons through the mitochondrial membrane, so that ATP synthesis and phosphate oxide decoupling decoupling. Thus, oxidative stress can be reduced and oxidative damage 106 can be prevented by maintaining ros stabilization. Among UCPP members, UCP2 is considered important for preventing oxidative stress108. Numerous studies have reported that increased UDP2 expression can reduce damage to oxidant tissue109. Furthermore, oxidative damage in the brain arteries that activate PPAR to fight aging is associated with the increase of UDP2110.
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结果 (英语) 3:[复制]
复制成功!
The migration of smooth muscle cells is an important reason for the formation of as, and oxidative stress is one of the main factors of VSMC proliferation and migration. In addition to xanthine oxidase, cyclooxygenase and lipoxygenase, uncoupled endothelial nitric oxide synthase, peroxidase and NADPH oxidase 103, mitochondrial enzymes are also major enzymes 104 and 105 for ROS production. Mitochondrial uncoupling proteins (UCPs) are proteins in the mitochondrial inner membrane, belonging to the superfamily of mitochondrial anion transporters. They decouple ATP synthesis from oxidative phosphorylation by controlling proton leakage through the mitochondrial intima. Thus, oxidative stress can be maintained to prevent oxidative damage. Among the members of UCP, UCP2 is considered to be important in the prevention of oxidative stress. A large number of studies have reported that increased UCP2 expression can reduce oxidant tissue damage 109. Moreover, activation of PPAR γ to resist oxidative damage in aging cerebral arteries is associated with upregulation of ucp2110.<br>
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