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首页> 外文期刊>Life sciences >Oxidized LDL from subjects with different dietary habits modifies atherogenic processes in endothelial and smooth muscle cells.
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Oxidized LDL from subjects with different dietary habits modifies atherogenic processes in endothelial and smooth muscle cells.

机译：来自不同饮食习惯的受试者的氧化低密度脂蛋白可改变内皮细胞和平滑肌细胞的动脉粥样硬化过程。

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Low-density lipoprotein (LDL) activates a number of processes involved in atherogenesis and vasoconstriction. Evidence suggests that oxidation increases the atherogenicity of LDL. We investigated the effects of oxidized LDL (ox-LDL) on cytotoxicity, prostacyclin (PGI2), and cyclic guanosine-3',5'-monophosphate (cGMP) production in rat vascular smooth muscle cell (VSMC) and rat heart endothelial cell (EC) culture, as well as EC- and VSMC-mediated LDL oxidation. Native LDL (n-LDL) was isolated from subjects on three long-term diets with differing fatty acid content (control diet rich in saturated fat and vegetarian and fish diets). The Cu2+-catalyzed oxidation of n-LDL was monitored using conjugated diene formation and stopped at various time points to achieve 20%, 45%, 70%, and 100% levels of ox-LDL. The lag phase of oxidation by Cu2+ was shortest and thiobarbituric acid-reactive substance (TBARS) formation by VSMC-mediated oxidation was highest with n-LDL obtained from the fish diet group. There were no differences between the ox-LDLs obtained from the different diet groups in their cytotoxicity in EC culture. The degree of oxidation did not influence LDL cytotoxicity. In VSMC culture PGI2 production was increased by ox-LDLs from all diet groups. In EC culture only the extensively oxidized LDLs obtained from the vegetarian diet group were able to induce PGI2 production. The LDLs did not affect basal cGMP production in either EC or VSMC culture.
机译：低密度脂蛋白（LDL）激活涉及动脉粥样硬化和血管收缩的许多过程。有证据表明，氧化会增加LDL的动脉粥样硬化性。我们研究了氧化LDL（ox-LDL）对大鼠血管平滑肌细胞（VSMC）和大鼠心脏内皮细胞（VSMC）中细胞毒性，前列环素（PGI2）和环状鸟苷3'，5'-单磷酸（cGMP）产生的影响EC）培养以及EC和VSMC介导的LDL氧化。天然低密度脂蛋白（n-LDL）是从受试者的三种长期饮食中分离出来的，这些长期饮食具有不同的脂肪酸含量（富含饱和脂肪，素食和鱼类饮食的对照饮食）。使用共轭二烯形成监测Cu- +催化的n-LDL氧化，并在各个时间点停止以达到ox-LDL 20％，45％，70％和100％的水平。从鱼饲料组获得的n-LDL，Cu2 +氧化的滞后阶段最短，而VSMC介导的氧化形成的硫代巴比妥酸反应性物质（TBARS）最高。从不同饮食组获得的ox-LDLs在EC培养物中的细胞毒性没有差异。氧化程度不影响LDL细胞毒性。在VSMC培养中，所有饮食组的ox-LDL均可增加PGI2的产量。在EC文化中，只有从素食饮食组中获得的广泛氧化的LDL能够诱导PGI2的产生。在EC或VSMC培养中，LDL均不影响基础cGMP的产生。

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