Mohan P F, Desaiah D
Department of Neurology, University of Mississippi Medical Center, Jackson 39216.
Biochem Biophys Res Commun. 1994 Nov 15;204(3):1047-54. doi: 10.1006/bbrc.1994.2568.
The effect of lipoproteins on rat peritoneal macrophage nitric oxide (NO) production was studied. Very low density (VLDL) and low density (LDL) but not high density lipoprotein (HDL) stimulated NO production at 12, 24 and 48 hr of incubation with macrophages. Forty-eight hour incubation of macrophages with VLDL or LDL increased NO production from 10.8 nmoles/10(6) cells in control to 249 and 60 nmoles/10(6) cells, respectively. VLDL-induced nitric oxide production was 825 nmoles/10(6) after 12 days of incubation. VLDL by itself or in the presence of LDL and HDL induced similar levels of NO in 24 hrs. Lipoproteins were without effect on NO, when incubated with macrophages in the absence of L-arginine and in the presence of nitric oxide synthase inhibitor monomethyl-L-arginine (L-NMMA). Oxidized VLDL was as effective as native form in the induction of macrophage NO, whereas oxidized LDL did not induce NO production. Further, the presence of 100 microM vitamin E in the incubation had no effect on VLDL- and LDL-induced NO production. Preincubation of macrophages with VLDL and LDL for 3hr or 6hrs activated macrophages to generate NO. These effects of lipoproteins could be of interest in the pathophysiology of lipoproteins and NO mediated diseases.
研究了脂蛋白对大鼠腹膜巨噬细胞一氧化氮（NO）产生的影响。极低密度脂蛋白（VLDL）和低密度脂蛋白（LDL）而非高密度脂蛋白（HDL）在与巨噬细胞孵育12、24和48小时时刺激了NO的产生。巨噬细胞与VLDL或LDL孵育48小时后，NO的产生分别从对照中的10.8纳摩尔/10⁶个细胞增加到249和60纳摩尔/10⁶个细胞。孵育12天后，VLDL诱导的一氧化氮产生量为825纳摩尔/10⁶。VLDL单独或在LDL和HDL存在的情况下在24小时内诱导产生相似水平的NO。当在无L-精氨酸且存在一氧化氮合酶抑制剂单甲基-L-精氨酸（L-NMMA）的情况下与巨噬细胞孵育时，脂蛋白对NO没有影响。氧化型VLDL在诱导巨噬细胞产生NO方面与天然形式一样有效，而氧化型LDL则不诱导NO产生。此外，孵育中存在100微摩尔维生素E对VLDL和LDL诱导的NO产生没有影响。巨噬细胞与VLDL和LDL预孵育3小时或6小时可激活巨噬细胞以产生NO。脂蛋白的这些作用可能在脂蛋白和NO介导的疾病的病理生理学中具有重要意义。
