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Tempol attenuates atherosclerosis associated with metabolic syndrome via decreased vascular inflammation and NADPH-2 oxidase expression

机译:Tempol通过减少血管炎症和NADPH-2氧化酶表达来减轻与代谢综合征相关的动脉粥样硬化

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Oxidative stress is an important factor in the generation of vascular injury in atherosclerosis. Chronic administration of fructose in rodents is able to facilitate oxidative damage. In the present study we evaluated the role of Tempol, a superoxide dismutase mimetic, on the effect of high fructose intake in apolipoprotein E-deficient (ApoE-KO) mice. Rodents were fed with fructose overload (FF, 10% w/v) for 8 weeks and treated with Tempol 1 mg/kg/day the latest 4 weeks. Tempol revert the pro-oxidant effects caused by FF, diminished lipid peroxidation and impaired vascular NADPH oxidase system through the downregulation of p47phox expression in the vascular wall. Tempol inhibited the expression of vascular adhesion molecule 1 (VCAM-1) in aorta and reduced the development of atheroma plaques. Our results indicate that tempol attenuates oxidative stress by interfering with the correct assembly of Nox2 oxidase complex in the vascular wall and is able to reduce atherosclerosis. Thus tempol represents a potential therapeutic target for preventing risk factors associated with metabolic syndrome.
机译:氧化应激是导致动脉粥样硬化血管损伤的重要因素。在啮齿动物中长期施用果糖能够促进氧化损伤。在本研究中,我们评估了超氧化物歧化酶模拟物Tempol对载脂蛋白E缺乏症(ApoE-KO)小鼠高果糖摄入量的影响。给啮齿动物喂食果糖超载(FF,10%w / v),持续8周,并在最近4周内以1 mg / kg /天的Tempol处理。 Tempol通过下调血管壁中p47phox的表达来逆转由FF引起的促氧化作用,减少脂质过氧化作用和损害血管NADPH氧化酶系统。 Tempol抑制了主动脉中血管粘附分子1(VCAM-1)的表达,并减少了斑块的形成。我们的结果表明,tempol通过干扰Nox2氧化酶复合物在血管壁中的正确组装来减轻氧化应激,并且能够减少动脉粥样硬化。因此,tempol代表了用于预防与代谢综合征相关的危险因素的潜在治疗靶标。

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