期刊文献+

非诺贝特对LPC诱导的人脐静脉内皮细胞增生、凋亡、NO生成及XIAP mRNA表达的影响

Effects of fenofibrate on proliferation,apoptosis,NO and XIAP expression induced by lysophosphatidylcholine in cultured human umbilical vein endothelial cells
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摘要 目的:探讨非诺贝特对LPC诱导的人脐静脉内皮细胞(HUVECs)增生、凋亡、NO生成及X连锁凋亡抑制蛋白(XIAP)mRNA表达的影响。方法:体外培养HUVECs株CRL-1730,分为正常对照组、LPC组、低浓度非诺贝特组(10μmol/L)、中浓度非诺贝特组(50μmol/L)、高浓度非诺贝特组(100μmol/L)。分别观测内皮细胞增生、凋亡、NO生成及XIAPmRNA表达的变化。结果:与正常对照组比较,LPC抑制CRL-1730细胞增生,促进凋亡,降低NO浓度,减弱XIAPmRNA的表达。非诺贝特干预后,CRL-1730细胞增生增强,凋亡减少,NO浓度升高,XIAPmR-NA表达增强,且其作用呈时间-效应、浓度-效应依赖关系。结论:非诺贝特可通过促进XIAP表达,干预LPC对HUVECs的影响,使内皮细胞增生增强,凋亡减少,NO浓度升高,从而起到抗动脉硬化作用。 Aim: To investigate the effects of fenofibrate on proliferation and apoptosis and XIAP expression induced by lysophosphatidylcholine in cultured human umbilical vein endothelial cells (HUVECs). Methods:HUVECs were cultured in vitro and allocated into 5 groups: normal control group, LPC group, low-concentration fenofibrate ( 10μmol/L) group, moderate-concentration fenofibrate (50 μmol/L)group and high-concentration fenofibrate (100 μmol/L)group. Proliferation and apoptosis of HUVECs were evaluated by MTT assay, flow cytometry (FCM) and fluorescence microscopy respectively. The expression of XIAP mRNA was examined by real time-PCR. Results : Compared with control group, LPC could inhibit the growth and induce apoptosis of HUVECs, and decrease NO production and the expression of XIAP mRNA in HUVECs. Fenofibrate could increase the growth and decrease the apoptosis of HUVECs, and enhance NO production and the expression of XIAP mRNA in HUVECs in a dose-and time-dependent way. Conclusion : Fenofibrate could improve the proliferation and decrease apoptosis of HUVECs induced by lysophosphatidylcholine by enhancing expression of XIAP mRNA in HUVECs, which may play an important role in the prevention and treatment of atherosclerosis.
出处 《郑州大学学报(医学版)》 CAS 北大核心 2006年第5期876-879,共4页 Journal of Zhengzhou University(Medical Sciences)
关键词 非诺贝特 人脐静脉内皮细胞 增生 凋亡 XIAP fenofibrate human umbilical vein endothelial cells proliferation apoptosis XIAP
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