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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,浙江杭州310003
出 处:《心脑血管病防治》2006年第4期223-226,共4页CARDIO-CEREBROVASCULAR DISEASE PREVENTION AND TREATMENT
摘 要:目的探讨前列腺素EI(prostaglandin EI,PGEI)对内皮细胞一氧化氮(NO)表达和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)为实验对象,检测不同浓度PGEI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PGEI浓度的升高,eNOS的活性和NO的含量均逐渐增加(P<0.05);(2)短时间PGEI的干预对eNOS和NO的影响均不明显,24h后细胞中eNOS活性明显升高(P<0.05),NO的含量自12h起随时间延长而增加(P<0.05);(3)用不同PGEI浓度预处理,使TNF-α对eNOS活动的抑制作用减弱。结论PGEI可能通过诱导eNOS的表达,促进NO的释放,且可以重新激活被TNF-α抑制的eNOS活性。Objective To evaluate the effects of PGE1 on Production of No and the activity of eNOS in human umbilical vein endothelial cells(HUVECs).Methods Nitric oxide (NO) production and the activity of nitric oxide synthase(NOS) in HUVECs were measured by No and NOS assay kits, after HUVECs incubated with PGE1 alone at different concentrations (0.04 - 0.4μg/ml) and different times(2- 4h) or HUVECs incubated with PGE1 as pretreatment before TNF- α 10ng/ml. Results ( 1 ) Activity of eNOS and the expression of NO were up- regulated by PGE1 in concentration-dependent manner. (2) Short time intervention with PGE1 lind little effects on both activity of eNOS and the expression of NO. However, the expression of NO was increased after 12h incubation and the activity of eNOS was enhanced after 24h treatment. (3) PGE1 could prevent eNOS activity inhibition induced by TNF - α. Conclusions PGE1 has a protection effect on endothelial cells by enhancing eNOS activity and increasing NO production, besides, it could prevent eNOS activity inhibition induced by TNF- α.
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