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机构地区:[1]湖北医科大学生物化学教研室,武汉430071
出 处:《中国动脉硬化杂志》1998年第3期198-201,共4页Chinese Journal of Arteriosclerosis
基 金:湖北省卫生厅资助
摘 要:为探讨脂蛋白(a)高度致动脉粥样硬化作用的可能机制,本文通过体外CU2+氧化法进行了低密度脂蛋白和脂蛋白(a)的氧化,并利用细胞计数及氚标胸腺密啶脱氧核苷掺入法,比较观察了天然和氧化的脂蛋白(a)及低密度脂蛋白对培养的兔主动脉平滑肌细胞增殖的影响。结果发现,在相同氧化时间内脂蛋白(a)对Cu2+的氧化敏感性较低密度脂蛋白低;氧化后的脂蛋白(a)和低密度脂蛋白均可明显促进平滑肌细胞增殖使DNA合成增加(P<0.01),且其作用较相应的天然脂蛋白大(P<0.05.P<0.01)、此结果提示:脂蛋白(a)经氧化后促进平滑肌细胞增殖可能是其致动脉粥样硬化的机制之一。Aim To identify possible mechanisms of the sug-gested high atherogenicity of lipoprotein (a) [LP(a)],the susceptibility of LP (a) to Cu2+-induced oxidation and its effects on proliferation of rabbit aortic smooth muscle cells (SMC) were studied and compared with those of low density lipoprotein (LDL).Methods Human Lp(a) and LDL were isolated and purified from normal blood plasma by ultracen-trifugation, sephacryl S-400 gelpermeation chromatog-raphy. The oxidative modification of Lp(a) and LDLwas identified by agarose gel electrophoresis and thio-barbituric acid reacitive substance(TBARS) method.Cell counting and 3H-TdR incorporation were used to observe the mitogenic effect of lipoproteins and oxi-dized lipoproteins on SMC.Results The susceptibility of LP (a) to oxidation was lower than that of LDL. Native Lp(a) and LDL induced slight increase in number of SMC and 3H-TdR incorporation respectively, which was statistically in-significant (P>0. 05); ox-Lp(a) and ox-LDL promot-ed the increase of cell number and DNA synthesis significantly (P<0. 01), and the promoting effects were greater than those of the corresponding native lipoproteins (P<0. 05, P<0. 01).Conclusion Oxidized LP (a) might play a role in atherogenesis through stimulating the proliferaion of SMC.
关 键 词:脂蛋白(a) 氧化型脂蛋白 主动脉平滑肌 细胞增殖
分 类 号:R543.502[医药卫生—心血管疾病] R363.14[医药卫生—内科学]
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