The mitochondria-targeted antioxidant MitoQ modulates oxidative stress, inflammation and leukocyte-endothelium interactions in leukocytes isolated from type 2 diabetic patients.
The mitochondria-targeted antioxidant MitoQ modulates oxidative stress, inflammation and leukocyte-endothelium interactions in leukocytes isolated from type 2 diabetic patients.
复制标题
靶向抗氧化剂MitoQ调节从2型糖尿病患者分离的白细胞中的氧化应激、炎症和白细胞-内皮细胞相互作用。
DOI：
10.1016/j.redox.2016.10.017
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发表时间：
2016-12
期刊：
影响因子：
11.4
通讯作者：
Victor, Victor M.
中科院分区：
文献类型：
--
作者：
Escribano-Lopez, Irene;Diaz-Morales, Noelia;Rovira-Llopis, Susana;de Maranon, Arantxa Martinez;Orden, Samuel;Alvarez, Angeles;Banuls, Celia;Rocha, Milagros;Murphy, Michael P.;Hernandez-Mijares, Antonio;Victor, Victor M.
目前尚不清楚线粒体靶向抗氧化剂如mito醌（MitoQ）是否可以调节T2D患者的氧化应激和白细胞-内皮细胞相互作用。我们的目的是评估MitoQ对T2D患者白细胞氧化应激参数和白细胞-内皮相互作用的有益作用。研究人群包括98例T2D患者和71例对照受试者。我们评估了代谢和人体测量参数、线粒体活性氧（ROS）产生、谷胱甘肽过氧化物酶1 （GPX-1）、NFκB-p65、TNFα和白细胞-内皮相互作用。糖尿病患者的体重、BMI、腰围、收缩压、舒张压、血糖、胰岛素、HOMA-IR、HbA1c、甘油三酯、hs-CRP和HDL-c均高于对照组。线粒体ROS的产生在T2D患者中增加，并通过MitoQ降低。抗氧化剂还能提高T2D患者GPX-1水平和PMN滚动速度，降低PMN滚动通量和PMN粘附。在T2D时，nf - κ b -p65和tnf - α升高，而MitoQ处理后两者均降低。我们的研究结果支持抗氧化剂MitoQ在T2D患者的白细胞中具有抗炎和抗氧化作用，通过NFκB的作用降低ROS的产生、白细胞-内皮相互作用和TNFα。这些数据表明，线粒体靶向抗氧化剂，如MitoQ，应该作为预防t2dm患者心血管事件的新手段进行研究。线粒体ROS的产生在糖尿病白细胞中增加，并被MitoQ减少。MitoQ治疗增加T2D白细胞GPX-1水平。MitoQ提高了PMN的轧制速度，降低了PMN的轧制通量和附着力。在T2D时，nf - κ b -p65和tnf - α升高，而MitoQ处理后两者均降低。应将MitoQ作为一种降低T2D患者心血管风险的新手段进行研究。
It is not known if the mitochondria-targeted antioxidants such as mitoquinone (MitoQ) can modulate oxidative stress and leukocyte-endothelium interactions in T2D patients. We aimed to evaluate the beneficial effect of MitoQ on oxidative stress parameters and leukocyte-endothelium interactions in leukocytes of T2D patients. The study population consisted of 98 T2D patients and 71 control subjects. We assessed metabolic and anthropometric parameters, mitochondrial reactive oxygen species (ROS) production, glutathione peroxidase 1 (GPX-1), NFκB-p65, TNFα and leukocyte-endothelium interactions. Diabetic patients exhibited higher weight, BMI, waist circumference, SBP, DBP, glucose, insulin, HOMA-IR, HbA1c, triglycerides, hs-CRP and lower HDL-c with respect to controls. Mitochondrial ROS production was enhanced in T2D patients and decreased by MitoQ. The antioxidant also increased GPX-1 levels and PMN rolling velocity and decreased PMN rolling flux and PMN adhesion in T2D patients. NFκB-p65 and TNFα were augmented in T2D and were both reduced by MitoQ treatment. Our findings support that the antioxidant MitoQ has an anti-inflammatory and antioxidant action in the leukocytes of T2D patients by decreasing ROS production, leukocyte-endothelium interactions and TNFα through the action of NFκB. These data suggest that mitochondria-targeted antioxidants such as MitoQ should be investigated as a novel means of preventing cardiovascular events in T2D patients. Mitochondrial ROS production was enhanced in diabetic leukocytes and reduced by MitoQ. MitoQ treatment increased GPX-1 levels in T2D leukocytes. MitoQ increased PMN rolling velocity and decreased PMN rolling flux and adhesion. NFκB-p65 and TNFα were augmented in T2D and were both reduced by MitoQ treatment. MitoQ should be investigated as a novel means of reducing cardiovascular risk in T2D.
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影响因子：
7.7
作者：
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通讯作者：
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影响因子：
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作者：
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DOI：
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