脂氧素A_4对脂多糖诱导巨噬细胞氧化损伤的影响  

Effects of Lipoxin A_4 on Lipopolysaccharide-induce Oxidative Damage in Macrophage

作　　者：周晓燕[1,2] 徐方云[1] 蔡震宇[1] 王红梅[1] 祝子瑞[1] 吴萍[2] 叶笃筠[2] 

机构地区：[1]南昌大学医学院病理生理系,南昌330006 [2]华中科技大学同济医学院病理生理系,武汉430030

出　　处：《细胞生物学杂志》2009年第3期433-436,共4页Chinese Journal of Cell Biology

基　　金：国家自然科学基金资助项目(No.30570726和No.30772154)~~

摘　　要：为了研究脂氧素(LXs)是否具备拮抗脂多糖(LPS)诱导巨噬细胞氧化损伤的作用,本文分别通过MTT法观察脂氧素A4(LXA4)对LPS损伤巨噬细胞活力的影响;流式细胞术检测活性氧(ROS)生成水平;试剂盒检测细胞内丙二醛(MDA)、一氧化氮(NO)的生成量及超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GSH-Px)、诱导型一氧化氮合酶(iNOS)的酶活性变化。结果表明LXA4可以提高LPS处理巨噬细胞的活力;减少ROS、NO、MDA的生成量;抑制iNOS的活性而增强SOD、GSH-Px、CAT抗氧化酶的活性。由些可见,LXA4可以通过抑制ROS及NO产生的同时增强抗氧化酶的活性而拮抗LPS所致的巨噬细胞氧化损伤。To study the effects of lipoxin lipopolysaccharide （LPS）, the cells were exposure A4 （LXA4） on oxidative damage of macrophages exposed to to LPS and different concentrations of LXA4. Then, the cell activity was analyzed by MTT assays; reactive oxygen species （ROS） were quantified through flow cytometry （FCM）; the levels of nitric oxide （NO） and malondialdehyde （MDA）, besides the activities of SOD, GSH-Px, CAT, and iNOS were all detected through assay kits. In this study, the data indicated LXA4 was able to increase the survival activity of LPS-treated macrophages; decrease the levels of ROS, NO and MDA; inhibit the activity of iNOS; promote the activity of SOD, GSH-Px, and CAT. It seemed that LXA4 could antagonize LPS-induced oxidative damage through decrease the production of ROS and NO but also increase the activity of antioxidative enzymes.

关 键 词：脂氧素 脂多糖 活性氧 氧化损伤 

分 类 号：R363[医药卫生—病理学]