雌二醇抑制系膜细胞介导的低密度脂蛋白氧化。

J Neugarten, C Ghossein, S Silbiger
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引用次数: 0

摘要

有研究表明,高脂血症可能通过氧化低密度脂蛋白(LDL)对肾小球系膜的有害作用而促进肾脏疾病的进展。由于雌激素具有强大的抗氧化活性,我们试图确定性激素是否影响肾小球系膜细胞对LDL的氧化。将大鼠系膜细胞与低密度脂蛋白(200微克/毫升)孵育,通过硫代巴比妥酸反应物质(TBARS)的产生、电泳迁移率的增加以及巨噬细胞对系膜细胞修饰LDL的摄取增强来评估脂质氧化程度。低密度脂蛋白与系膜细胞孵育时,观察到TBARS的逐渐升高和电泳迁移率的增加。与雌二醇(10 μ mol/L)共孵育36小时,使TBARS生成减少46% (p < 0.01),并逆转了相对电泳迁移率的增加(1.25 +/- 0.07 vs 1.01 +/- 0.03, p < 0.05)。在雌二醇(10 μ mol/L)存在的情况下,被系膜细胞氧化的LDL与在没有雌二醇的情况下被系膜细胞氧化的LDL相比,巨噬细胞的摄取减少(每小时14 +/- 2 pmol/10(6)个细胞vs 22 +/- 3 pmol/10(6)个细胞,p < 0.05)。相比之下,睾酮和雌酮对这些参数都没有任何影响。我们得出结论,雌二醇凭借其抗氧化特性,抑制系膜细胞介导的LDL氧化,并减少巨噬细胞对系膜细胞修饰LDL的摄取。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Estradiol inhibits mesangial cell-mediated oxidation of low-density lipoprotein.

It has been suggested that hyperlipidemia may contribute to the progression of renal disease via the deleterious effects of oxidized low-density lipoprotein (LDL) on the glomerular mesangium. Because estrogens possess potent antioxidant activity, we sought to determine whether sex hormones influence the oxidation of LDL by mesangial cells. Rat mesangial cells were incubated with LDL (200 micrograms/ml), and the extent of lipid oxidation was assessed by the generation of thiobarbituric acid reactive substances (TBARS), by increased electrophoretic mobility, and by enhanced uptake of mesangial cell-modified LDL by macrophages. A progressive rise in TBARS and an increase in electrophoretic mobility was observed on incubation of LDL with mesangial cells. Coincubation with estradiol (10 mumol/L) reduced TBARS generation by 46% at 36 hours (p < 0.01) and reversed the increase in relative electrophoretic mobility (1.25 +/- 0.07 vs 1.01 +/- 0.03, p < 0.05). LDL that had been oxidized by mesangial cells in the presence of estradiol (10 mumol/L) showed reduced uptake by macrophages when compared with LDL that had been oxidized by mesangial cells in the absence of estradiol (14 +/- 2 pmol/10(6) cells per hour vs 22 +/- 3 pmol/10(6) cells per hour, p < 0.05). In contrast, neither testosterone nor estrone had any effect on these parameters. We conclude that estradiol, by virtue of its antioxidant properties, inhibits mesangial cell-mediated oxidation of LDL and reduces the uptake of mesangial cell-modified LDL by macrophages.

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