甲基莲心碱抑制氧化极低密度脂蛋白的形成及其生物学效应  

Inhibition of Very Low Density Lipoprotein Oxidation by Neferine and Its Biologic Effect

作　　者：冯友梅[1] 吴捷莉[1] 从容[1] 宗义强[1] 王淳本[1] 冯宗忱[1] 

机构地区：[1]同济医科大学基础医学院生物化学教研室

出　　处：《同济医科大学学报》1999年第2期89-91,共3页Acta Universitatis Medicinae Tongji

摘　　要：采用Ｃｕ２＋在体外氧化极低密度脂蛋白（ＶＬＤＬ），用甲基莲心碱（Ｎｅｆ）作抗氧化剂。将脂蛋白分为正常、氧化和Ｎｅｆ抗氧化三组，测定脂蛋白的硫代巴比妥酸反应物质（ＴＢＡＲＳ）。结果分别为（０．６１±０．０３）、（６．０８±０．２５）和（２．３３±０．９１）μｍｏｌ／ｇ蛋白，每二组间的差异均有显著性（Ｐ＜０．０１）。氧化和Ｎｅｆ抗氧化的ＶＬＤＬ与巨噬细胞（ＭΦ）在３７℃温育４８ｈ后，ＭΦ内甘油三酯（ＴＧ）和总胆固醇（ＴＣ）含量显示前者比后者有更强的促进ＭΦ内脂质堆积的作用（Ｐ＜０．０５）。研究结果表明。Oxidatively modified very low density lipoprotein (Ox VLDL) enhances the formation of macrophage derived foam cell. To investigate the role of neferine (Nef) in anti VLDL oxidation and foam cell formation, the lipoprotein was divided and subjected to three different treatments: N VLDL(native VLDL), Ox VLDL(Cu 2+ +VLDL) and Cu 2+ +Nef+VLDL. The VLDLs were put at 25 ℃ for 24 h and the thiobarbituric acid reactive substance(TBARS) values were determined. TBARs values were (0.61±0.03), (6.08±0.25) and (2.33±0.91) nmol/mg protein, respectively with the difference being very significant( P <0.01) for each two groups. Mouse peritoneal macrophage(MΦ) were exposed to 50 mg protein/L of Ox VLDL and Cu 2+ +Nef+VLDL at 37 ℃ for 48 h, respectively. The tryglyceride (TG) and total cholesterol(TC) content in MΦ were assayed. The results showed that Ox VLDL was more efficient than Cu 2+ +Nef+VLDL in stimulating lipid accumulation in MΦ ( P <0.05).The study demonstrates that Nef can inhibit Cu 2+ mediated VLDL oxidation and by which inhibit macrophage derived foam cell formation.

关 键 词：甲基莲心碱 极低密度脂蛋白 氧化 生物学效应 

分 类 号：R286.9[医药卫生—中药学] Q513.5[医药卫生—中医学]