Role of arterial wall antioxidant defense in beneficial effects of exercise on atherosclerosis in mice
Role of arterial wall antioxidant defense in beneficial effects of exercise on atherosclerosis in mice
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DOI：
10.1161/hq1001.097106
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发表时间：
2001-10-01
影响因子：
8.7
通讯作者：
Parthasarathy, S
中科院分区：
文献类型：
--
作者：
Meilhac, O;Ramachandran, S;Parthasarathy, S
运动降低动脉粥样硬化风险的机制仍不清楚。这项研究检验了以下假设：持续运动引起的氧化应激可能会增强动脉壁的抗氧化防御能力。与久坐的对照小鼠相比，急性运动导致正常小鼠主动脉壁中氧化修饰蛋白和过氧化氢酶的抗体增加。在雄性动脉粥样硬化饮食喂养的低密度脂蛋白 (LDL) 受体缺陷小鼠中，与久坐的对照小鼠相比，运动可降低血浆胆固醇 (15%)，并使动脉粥样硬化病变减少 40%，同时动脉过氧化氢酶和内皮 NO 合酶增加。由于这些小鼠缺乏 LDL 受体，因此结果表明 LDL 受体可能与运动引起的血浆胆固醇降低无关。与未治疗的运动小鼠中的病变形成相比，对运动中的 LDL 受体缺陷小鼠补充维生素 E 并没有显着减少动脉粥样硬化病变的形成。此外，维生素E通过阻止主动脉过氧化氢酶活性和内皮NO合酶表达的诱导来抵消运动的有益效果。这些结果可能表明，尽管维生素 E 可能可以预防运动引起的氧化应激，但其在动脉中的可用性不足以预防动脉粥样硬化过程。这些结果表明，运动引起的血浆氧化应激可能通过刺激动脉抗氧化反应来预防动脉粥样硬化。此外，补充维生素 E 可能会抑制动脉壁中抗氧化酶的积聚，从而对锻炼者有害。
The mechanism(s) by which exercise reduces atherogenic risk remains unknown. This study tested the hypothesis that sustained exercise-induced oxidative stress may increase antioxidant defense in the arterial wall. Acute exercise induced an increase in antibodies to oxidatively modified proteins and catalase in the aortic walls of normal mice compared with sedentary control mice. In male atherogenic diet-fed low density lipoprotein (LDL) receptor-deficient mice, exercise lowered plasma cholesterol (15%) and decreased atherosclerotic lesions by 40% compared with values in sedentary control mice, with a concomitant increase in arterial catalase and endothelial NO synthase. Because these mice lack the LDL receptor, the results indicate that the LDL receptor might not be responsible for the exercise-induced lowering of plasma cholesterol. Vitamin E supplementation to exercising LDL receptor-deficient mice did not reduce atherosclerotic lesion formation significantly as opposed to lesion formation in untreated exercised mice. Moreover, vitamin E counteracted the beneficial effects of exercise by preventing the induction of aortic catalase activity and endothelial NO synthase expression. These results might indicate that although vitamin E might have prevented the exercise-induced oxidative stress, its availability in the artery was insufficient to prevent the atherosclerotic process. These results indicate that exercise-induced plasma oxidative stress could be responsible for the prevention of atherosclerosis by stimulating arterial antioxidant response. Furthermore, vitamin E supplementation could be deleterious in exercisers by inhibiting antioxidant enzyme buildup in the arterial wall.