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氧化低密度和极低密度脂蛋白对鼠腹腔巨噬细胞的增殖作用 被引量:2

THE EFFECTS OF OXIDATIVE MODIFIED LOW DENSITY AND VERY LOW DENSITY LIPOPROTEINS ON THE PROLIFERATION OF MURINE PERITONEAL MACROPHAGES
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摘要 巨噬细胞源性泡沫细胞增殖在动脉粥样硬化 (As)的形成过程中起重要作用 .用形态学、细胞计数、MTT掺入法和氚标胸腺嘧啶脱氧核苷 ( 3H TdR)掺入实验观察比较了氧化修饰脂蛋白 (Ox LDL ,Ox VLDL)和相应的天然型脂蛋白对培养的鼠腹腔巨噬细胞增殖的影响 .结果发现 ,Ox LDL和Ox VLDL均能显著刺激巨噬细胞内DNA合成增加促进细胞增殖 (与天然脂蛋白相比 ,P <0 .0 0 1) ,其中Ox VLDL的作用最为明显 (与Ox LDL相比P <0 .0 5) ;低浓度的氧化型脂蛋白 (蛋白浓度 0~ 5mg/L)促巨噬细胞呈剂量依赖性增殖 ,浓度为 5mg/L时 ,达到最高峰 ,随着浓度的进一步增加 ,促增殖作用逐渐减弱 ;而天然LDL及VLDL不能促进巨噬细胞增殖 .上述结果表明 ,与Ox LDL相似 ,Ox VLDL促进巨噬细胞增殖可能是其致As的机制之一 . The proliferation of macrophage derived foam cells plays an important role in the progression of the early stage of atherosclerosis. To study the effects of oxidative modified low density and very low density lipoproteins (Ox LDL and Ox VLDL) on the proliferation of murine peritoneal macrophages, macrophage growth was evaluated by morphological observation, cell counting assay, MTT assay and 3H thymidine incorporation assay after macrophages were incubated with various oxidized and native lipoproteins for 5 days. We found that both Ox LDL and Ox VLDL could significantly induce cellular DNA synthesis and stimulate macrophage proliferation (compared with native lipoprotein, P <0.001). When compared at 5?μg/mL, Ox VLDL was much more potent than Ox LDL in its growth stimulating activity ( P <0.05). In addition, like Ox LDL, Ox VLDL promoted macrophage growth in a dose dependent manner at concentrations<5?μg/mL, and showed the largest mitogenic activity at 5?μg/mL, followed by a decline to the basal lever at >40?μg/mL. In contrast, the growth of these cells was not stimulated by native lipoproteins. These in vitro data revealed the capacity of Ox VLDL , like Ox LDL, to induce growth of macrophage cells, indicating that the growth stimulating capacity of the Ox VLDL might be one of its atherogenic mechanisms.
出处 《南京大学学报(自然科学版)》 CAS CSCD 2000年第5期614-618,共5页 Journal of Nanjing University(Natural Science)
基金 军队医药卫生科研基金(98H005)
关键词 脂蛋白 氧化修饰 小鼠 巨噬细胞 增殖 lipoproteins oxidative modification, mice, macrophages proliferation
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