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作 者:刘术娟[1] 邱近明[1] 项建梅[2] 赵晖[1]
机构地区:[1]天津医科大学病理学教研室,300070 [2]天津医科大学内分泌研究所,300070
出 处:《天津医药》2001年第6期356-358,F003,共4页Tianjin Medical Journal
摘 要:目的:研究巨噬细胞对低密度脂蛋白(LDL)的修饰和前列腺素E_2(PGE_2)对动脉粥样硬化形成的抑制作用。方法:以巨噬细胞(Mp)作用LDL,并设PGE_2(20 mg/L)组,检测每组过氧化脂质含量,谷胱甘肽过氧化物酶活性,及形态计量学测定细胞变化和含脂量。结果:细胞修饰组的脂质过氧化物含量高于给PGE_2组,而谷胱甘肽过氧化物酶活性显著低于给药组。作用24小时的修饰组细胞面积明显增大,摄脂增加,均分别显著高于给药组和细胞对照组。结论:提示Mp能够氧化修饰LDL并能摄取脂质,导致泡沫细胞形成。大剂量PGE_2有抗LDL氧化修饰,抑制Mp细胞摄脂,和泡沫细胞形成,从而抑制动脉粥样硬化发生的作用。Objective:To study the modificatory effect of macrophages on low density lipoprotein (LDL) and the inhibitive effect of prostaglandin E2 (PGE2) on atherogenesis. Methods:The LDL was incubated in Ham's F10 medium with macrophages,or with macrophages and PGE2 (20 mg/L). The modifying changes of LDL were examined with biochemical,immunocytoche-mical and morphometric methods. Results:Compared with the PGE2 group, the content of lipid peroxide markedly increased and the activity of glutathione peroxidase was much lower in the modifying group. Through oil red O staining and morphometric study, the average area of macrophages and the lipid-laden cells were much larger in the modifying group than those in the PGE2 and control groups. Conclusion:Macrophages can modify LDL and accelerate foam cell formation. A large dose of PGE2 possessed a marked anti-atherogenesis function during early stage of atherosclerosis.
关 键 词:巨噬细胞 地诺前列酮 低密度脂蛋白 动脉粥样硬化 实验研究
分 类 号:R543.5[医药卫生—心血管疾病]
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