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目的 研究异丹叶大黄素 (Iso)对Cu2 + 介导的人低密度脂蛋白 (LDL)过氧化及氧化LDL(ox LDL)对小鼠巨噬细胞毒性的抑制作用。方法 用序贯超离心法分离血脂正常的供血者血清LDL ,分离的LDL 1mg·mL- 1磷酸缓冲液 (pH 7 4) ,与 10μmol·L- 1CuSO4 于 3 7℃水浴温育 10h以引起LDL过氧化 ,给药组预先加入不同浓度Iso ,对照组加等量生理盐水 ,测定丙二醛(MDA)的生成量、维生素E的耗竭以及LDL电泳迁移率。另外测定用ox LDL处理小鼠腹腔巨噬细胞线粒体的膜电位、吞噬刚果红及释放NO的量。结果 1-10 0 μmol·L- 1Iso剂量依赖性地抑制Cu2 + 引起的人LDL氧化时MDA的生成量、维生素E的耗竭及电泳迁移率的升高。 10 μmol·L- 1Iso能防止 0 1mg·mL- 1ox LDL与小鼠腹腔巨噬细胞温育 4h后线粒体膜电位的损伤、吞噬刚果红功能以及NO释放量的降低。结论 Iso在体外对Cu2 + 介导的LDL过氧化以及ox LDL对小鼠巨噬细胞的毒性有保护作用。
Objective To study the inhibitory effect of isoflavone emodin (Iso) on Cu2 +-mediated human low-density lipoprotein (LDL) peroxidation and oxidized LDL (ox LDL) on macrophage toxicity in mice. Methods Serum LDL was separated by sequential ultracentrifugation from donors with normal serum lipids. The isolated LDL 1 mg·mL -1 phosphate buffer (pH 74) was incubated with 10 μmol·L - 1 CuSO4 in a water bath at 37°C for 10 h to induce LDL. Peroxidation, the treatment group was pretreated with different concentration of Iso, and the control group was added with the same amount of physiological saline to determine the production of malondialdehyde (MDA), the depletion of vitamin E, and the electrophoretic mobility of LDL. In addition, the mitochondrial membrane potential of peritoneal macrophages was treated with ox LDL, and Congo red was engulfed and the amount of NO released. RESULTS 1-10 μmol·L-1Iso inhibited the production of MDA, the depletion of vitamin E and the increase of electrophoretic mobility in a dose-dependent manner. 10 μmol·L-1 Iso prevented the damage of mitochondrial membrane potential, phagocytosis of Congo red, and decrease of NO release after incubation with mouse peritoneal macrophages at 0 1 mg·mL-Lox for 4 h. Conclusion Iso can protect Cu2 + -mediated LDL peroxidation and ox LDL toxicity on mouse macrophages in vitro.