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机构地区:[1]湖南医科大学分子药理研究室
出 处:《中国药理学报》1997年第6期525-528,共4页Acta Pharmacologica Sinica
摘 要:目的:研究氧化型低密度脂蛋白(oxLDL)诱导血管和心内膜内皮细胞凋亡.方法:用超速离心法分离健康人血浆低密度脂蛋白(LDL),以CuSO410μmol·L-1氧化.观察oxLDL对培养新生小牛主动脉内皮细胞及心内膜细胞的损伤作用.琼脂糖凝胶电泳和Hoechst33258荧光密度法定性与定量分析DNA降解.结果:oxLDL诱导血管内皮细胞及心内膜细胞典型凋亡形态学改变,DNA降解呈时间和剂量依赖性.环己米特和硫酸葡聚糖对此作用无影响.BHT20μmol·L-1可取消DNA降解.溶血性磷脂酰胆碱50μmol·L-1无诱导凋亡作用.oxLDL诱导的DNA降解可被依他酸取消.结论:oxLDL诱导血管内皮细胞及心内膜细胞凋亡.IM: To examine whether oxidized low density lipoproteins (ox LDL) might induce apoptosis in bovine aortic and endocardial endothelial cells (BAEC and BEEC). METHODS: Low density lipoproteins (LDL) were isolated from healthy human plasma by ultracentrifugation and oxidized by CuSO 4 10 μmol·L -1 . BAEC and BEEC were incubated in a medium containing ox LDL, LDL, or phosphate buffer solution (PBS) as control. DNA fragmentation was visualized by agarose gel electrophoresis and determined quantitatively using Hoechst 33258 fluorochrome. RESULTS: Ox LDL, not LDL, elicited typical apoptotic changes and DNA fragmentation in BAEC and BEEC. In BAEC, dextran sulfate, and cicloheximide (Cic) exhibited no effect on DNA fragmentation induced by ox LDL. Butylated hydroxytoluene (BHT) 20 μmol·L -1 completely inhibited Cu 2+ mediated oxidation of LDL as well as the apoptosis inducing effect of Cu 2+ exposed LDL. Lysophosphatidylcholine (LPC) did not elicit DNA fragmentation in BAEC and in BEEC. DNA fragmentation induced by ox LDL in BAEC and in BEEC was blocked by chelating the calcium of the culture medium by egtazic acid. CONCLUSION: Ox LDL induces apoptosis in BAEC and BEEC without involving the LPC.)
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