Liu S X, Chen Y, Zhou M, Wan J
Research Laboratory of Free Radical Medicine, The First Military Medical University, Guangzhou, People's Republic of China.
Atherosclerosis. 1998 Jan;136(1):43-9. doi: 10.1016/s0021-9150(97)00185-8.
Previous work has shown that oxidized low density lipoprotein (Ox-LDL) inhibited lipopolysacchride (LPS)-induced nitric oxide (NO) production in macrophages. In this paper, the role of different components of Ox-LDL in the inhibitory effect was studied by measuring nitrite in media. Ox-LDL inhibited LPS-induced NO production in macrophage cell line J774.A1. When compared with Ox-LDL, native and acetylated LDL had a lesser effect on NO production. Pre-clearance of lipid hydroperoxides (LOOH) in Ox-LDL and removal of soluble thiobarbituric acid reactive substances (TBARS) in Ox-LDL solution by dialysis had no influence on the inhibitory effect of Ox-LDL. The protein moiety of Ox-LDL had no effect on NO production, but the lipid moiety inhibited NO production to about the same extent as intact Ox-LDL. Linoleic acid and phosphatidylcholine, the main components of LDL lipid, whether oxidized separately or together, had no effect on NO production. However, if linoleic acid and cholesterol oxidized together, there was very strong inhibition of NO production. Cholesterol oxidized alone also had some inhibitory effect. These results suggest that oxidized cholesterol in Ox-LDL might be responsible for the inhibition of NO production in macrophages.
先前的研究表明，氧化型低密度脂蛋白（Ox-LDL）可抑制巨噬细胞中脂多糖（LPS）诱导的一氧化氮（NO）生成。本文通过检测培养基中的亚硝酸盐，研究了Ox-LDL不同成分在这种抑制作用中的作用。Ox-LDL抑制巨噬细胞系J774.A1中LPS诱导的NO生成。与Ox-LDL相比，天然和乙酰化低密度脂蛋白对NO生成的影响较小。通过透析预先清除Ox-LDL中的脂质氢过氧化物（LOOH）以及去除Ox-LDL溶液中的可溶性硫代巴比妥酸反应性物质（TBARS），对Ox-LDL的抑制作用没有影响。Ox-LDL的蛋白质部分对NO生成没有影响，但脂质部分对NO生成的抑制程度与完整的Ox-LDL大致相同。LDL脂质的主要成分亚油酸和磷脂酰胆碱，无论是单独氧化还是一起氧化，对NO生成均无影响。然而，如果亚油酸和胆固醇一起氧化，则对NO生成有很强的抑制作用。单独氧化的胆固醇也有一定的抑制作用。这些结果表明，Ox-LDL中的氧化胆固醇可能是抑制巨噬细胞中NO生成的原因。
