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首页> 外文期刊>Life sciences >Effect of antioxidant in endothelial cells exposed to oxidized low-density lipoproteins.
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Effect of antioxidant in endothelial cells exposed to oxidized low-density lipoproteins.

机译：抗氧化剂对暴露于氧化的低密度脂蛋白的内皮细胞的影响。

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Antioxidants such as probucol and alpha-tocopherol have been shown to attenuate the oxidation of low-density lipoproteins (LDL) and atherosclerotic lesions in animal models of atherosclerosis. The purpose of this study is to determine the protection effect of antioxidants on endothelial cells when exposed to oxidized and native LDL. In a cell-free system, we found that probucol, alpha-tocopherol, and ascorbic acid inhibited copper-induced LDL oxidation by a dose-dependent fashion (from 1 microM to 10 mM). In porcine aortic endothelial cells, antioxidants alone did not change basal endothelin-1 (ET-1) secretion. When porcine aortic endothelial cells were exposed to LDL and oxidized-LDL, both of them stimulated ET-1 secretion dose-dependently, whereas oxidized-LDL elicited higher ET-1 secretion. However, probucol, alpha-tocopherol, and ascorbic acid did not prevent LDL or oxidized-LDL induced ET-1 secretion. Furthermore, nimodipine inhibited both of native and oxidized LDL induced ET-1 secretion. Since Ca2+ channel blocker reduced the elevation of induced ET-1 secretion, the [Ca2+]i is possibly involved for the regulation of ET-1 secretion. Our results suggest that antioxidants can only prevent the oxidation of LDL rather than oxidized and native LDL-induced ET-1 secretion in vascular endothelial cells. The increase in the [Ca2+]i of endothelial cells through the opening of voltage-dependent Ca2+ channels may be involved in the LDL-induced ET-1 release.
机译：在动脉粥样硬化的动物模型中，已证明抗氧化剂（如普罗布考和α-生育酚）可减弱低密度脂蛋白（LDL）和动脉粥样硬化病变的氧化。这项研究的目的是确定抗氧化剂暴露于氧化的和天然的LDL时对内皮细胞的保护作用。在无细胞系统中，我们发现普罗布考，α-生育酚和抗坏血酸以剂量依赖的方式（从1 microM到10 mM）抑制铜诱导的LDL氧化。在猪主动脉内皮细胞中，单独的抗氧化剂不会改变基础内皮素1（ET-1）的分泌。当猪主动脉内皮细胞暴露于低密度脂蛋白和氧化的低密度脂蛋白时，它们两者均剂量依赖性地刺激ET-1的分泌，而氧化的低密度脂蛋白则引起较高的ET-1分泌。但是，普罗布考，α-生育酚和抗坏血酸不能阻止LDL或氧化的LDL诱导ET-1分泌。此外，尼莫地平抑制天然和氧化的LDL诱导的ET-1分泌。由于Ca2 +通道阻滞剂降低了诱导的ET-1分泌的升高，因此[Ca2 +] i可能参与了ET-1分泌的调节。我们的研究结果表明，抗氧化剂只能阻止LDL的氧化，而不能阻止血管内皮细胞中LDL诱导的天然氧化和ET-1分泌。通过打开电压依赖性Ca 2+通道，内皮细胞[Ca 2+] i的增加可能与LDL诱导的ET-1释放有关。

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