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机构地区:[1]浙江大学医学院附属第一医院心内科
出 处:《浙江医学》2006年第8期636-638,684,共4页Zhejiang Medical Journal
摘 要:目的讨论肿瘤坏死因子-α(TNF-α)对内皮细胞一氧化氮(NO)产生及内皮型一氧化氮合酶(eNOS)活性的影响。方法以人脐静脉内皮细胞(HUVEC)为实验材料,检测与不同浓度TNF-α作用不同时间后,细胞培养上清液和细胞中NO水平的变化,以及细胞eNOS活性的改变。结果(1)随着TNF-α浓度的升高,eNOS的活性减弱,而细胞和上清液中NO的含量增加;(2)随着干预时间的延长,eNOS的活性减弱;而细胞和上清液中NO的含量在作用24h后升高,且明显高于对照组;(3)L-单甲基精氨酸(L-NMMA)和地塞米松(DXM)均能阻断TNF-α引起的细胞和细胞上清中NO的表达增加。结论TNF-α降低eNOS活性,却在高浓度和长时间作用后增加NO的合成,可能与激活诱导型一氧化氮合酶有关,因为NO的变化可以被L-NMMA和DXM阻断。Objective To investigate the effect of TNF-α on production of nitric oxide (NO) and activity of nitric oxide synthase(eNOS) in human umbilical vein endothelial cells(HUVECs). Methods HUVECs were incubated with TNF-α at different concentrations (2-20ng/ml) and different times(2-48h) or pretreatment with L-NMMA or DXM. Nitric oxide production and activity of nitric oxide synthase in HUVECs were measured by NO and NOS assay kits. Resuits (1) Activity of eNOS was down-regulated by TNF-α in a concentration-dependent manner, while production of NO was upregulated. (2) The activity of eNOS attenuated after long-time treatment with TNF-α, but marked increased production of NO was detected after 24h. (3) The induction of NO by TNF-α can be inhibited by L-NMMA and DXM. Conclusion TNF-α can reduce activity of eNOS and induce iNOS, so that production of NO is increased.
关 键 词:肿瘤坏死因子-Α 人脐静脉内皮细胞 一氧化氮 内皮型一氧化氮合酶
分 类 号:R543[医药卫生—心血管疾病]
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