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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Inhibition of rat lipoprotein lipid peroxidation by the oral administration of D003, a mixture of very long-chain saturated fatty acids.
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Inhibition of rat lipoprotein lipid peroxidation by the oral administration of D003, a mixture of very long-chain saturated fatty acids.

机译：口服D003（一种非常长链的饱和脂肪酸的混合物）可抑制大鼠脂蛋白脂质过氧化。

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Previous results have demonstrated that policosanol, a mixture of aliphatic primary alcohols isolated and purified from sugar cane wax, whose main component is octacosanol, inhibited lipid peroxidation in experimental models and human beings. D003 is a defined mixture of very long-chain saturated fatty acids, also isolated and purified from sugar cane wax, whose main component is octacosanoic acid followed by traicontanoic, dotriacontanoic, and tetracontanoic acids. Since very long-chain fatty acids are structurally related to their corresponding alcohols, we investigated the effect of oral treatment with D003 (0.5, 5, 50, and 100 mg/kg) over 4 weeks in reducing the susceptibility of rat lipoprotein to oxidative modification. The combined rat lipoprotein fraction VLDL + LDL was subjected to several oxidation systems, including those containing metal ions (CuSO4), those having the capacity to generate free radicals 2,2-azobis-2-amidinopropane hydrochloride (AAPH), and a more physiological system (resident macrophages). D003 (5, 50, and 100 mg/kg) significantly inhibited copper-mediated conjugated-diene generation in a concentration-dependent manner. D003 increased lag phase by 53.1, 115.3, and 119.3%, respectively, and decreased the rate of conjugate-diene generation by 16.6, 21.5, and 19.6%, respectively. D003 also inhibited azo-compound initiated and macrophage-mediated lipid peroxidation as judged by the significant decrease in thiobarbituric acid reactive substance (TBARS) generation. In all the systems the maximum effect was attained at 50 mg/kg. There was also a parallel attenuation in the reduction of lysine amino groups and a significant reduction of carbonyl content after oxidation of lipoprotein samples. Taken together, the present results indicate that oral administration of D003 protects lipoprotein fractions against lipid peroxidation in the lipid as well in the protein moiety.
机译：先前的研究结果表明，从甘蔗蜡中分离纯化的脂族伯醇混合物，即聚二十烷醇，其主要成分为十八烷醇，在实验模型和人类中均能抑制脂质过氧化。 D003是很长链的饱和脂肪酸的定义混合物，也可以从甘蔗蜡中分离和纯化，其主要成分是十八烷二酸，其次是二十三烷酸，四十三烷酸和四十六烷酸。由于非常长链的脂肪酸在结构上与其相应的醇有关，因此我们研究了在4周内口服D003（0.5、5、50和100 mg / kg）对降低大鼠脂蛋白对氧化修饰的敏感性的作用。将合并的大鼠脂蛋白级分VLDL + LDL进行几种氧化系统处理，包括那些包含金属离子（CuSO4），能够产生自由基2,2-偶氮二-2--2-基丙烷盐酸盐（AAPH）的氧化系统以及更具生理性的氧化系统系统（常驻巨噬细胞）。 D003（5、50和100 mg / kg）以浓度依赖的方式显着抑制铜介导的共轭二烯的生成。 D003分别使滞后相增加了53.1％，115.3％和119.3％，并使共轭二烯的生成速率分别减少了16.6％，21.5％和19.6％。 D003还抑制了偶氮化合物引发的巨噬细胞介导的脂质过氧化作用，这可以通过硫代巴比妥酸反应性物质（TBARS）生成的显着减少来判断。在所有系统中，最大效果达到50 mg / kg。脂蛋白样品氧化后，赖氨酸氨基的还原也平行减弱，羰基含量显着降低。综上所述，目前的结果表明，口服给予D003可保护脂蛋白组分抵抗脂质以及蛋白质部分中的脂质过氧化。

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