前列地尔对缺氧损伤的人肺微血管内皮细胞中VEGF和eNOS表达的影响 点击下载
论文标题: 前列地尔对缺氧损伤的人肺微血管内皮细胞中VEGF和eNOS表达的影响
英文标题:
中文摘要: 目的:研究前列地尔对缺氧损伤的人肺微血管内皮细胞(HPMECs)中血管内皮生长因子(VEGF)和内皮型一氧化氮合成酶(eNOS)表达的影响。方法:将HPMECs分为A组(正常培养)、B组(3%O2培养)、C组(3%O2培养+15 μg/L前列地尔)及D组(3%O2培养+45 μg/L前列地尔),相应培养24 h。观察各组细胞形态,MTT比色法检测细胞活力(以吸光度计),流式细胞仪检测细胞凋亡率,Western blot法检测细胞中VEGF、eNOS相对表达量。结果:A、D组细胞密度较高,B、C组细胞密度较低。与A组比较,B、C、D组细胞活力降低、凋亡率升高、VEGF与eNOS表达增强、eNOS/VEGF减少(P<0.05)。与B组比较,C、D组细胞活力增加、VEGF表达减弱(P<0.05);D组细胞凋亡率降低、eNOS表达减弱、eNOS/VEGF增加(P<0.05)。与C组比较,D组细胞凋亡率降低、VEGF表达减弱、eNOS/VEGF增加(P<0.05)。结论:前列地尔可能通过上调HPMECs的eNOS/VEGF发挥保护作用。
英文摘要: OBJECTIVE: To study the effects of alprostadil on the expression of vascular endothelial growth factor (VEGF) and endothelial nitric oxide synthase (eNOS) in human pulmonary microvascular endothelial cells (HPMECs) with hypoxia-induced injury. METHODS: HPMECs were divided into group A (normal cultural environment), group B (3%O2), group C (3%O2+15 μg/L alprostadil) and group D (3%O2+45 μg/L alprostadil) for 24 h culture. Cell morphology was observed; MTT method was conducted to detect cell activity (recorded by absorbance); flow cytometry was adopted to detect apoptosis rate; Western blot was used to detect relative expressions of VEGF and eNOS in cells. RESULTS: Cell density in group A and D was relatively high, that in group B and C was low. Compared with group A, cell activities decreased and apoptosis rates increased in group B, C and D, expressions of VEGF and eNOS enhanced, eNOS/VEGF decreased (P<0.05). Compared with group B, cell activities increased in group C and D, VEGF expression decreased (P<0.05); apoptosis rate in group D decreased, eNOS expression decreased and eNOS/VEGF increased. Compared with group C, cell apoptosis rate was decreased in group D, VEGF expression decreased and eNOS/VEGF increased (P<0.05). CONCLUSIONS: Alprostadil maybe play effect on HPMECs with hypoxia-induced injury by up-regulating the expression level of eNOS/VEGF.
期刊: 2016年第27卷第25期
作者: 王友俊,张玲美
英文作者: WANG Youjun,ZHANG Lingmei
关键字: 前列地尔;缺氧损伤;人肺微血管内皮细胞;血管内皮生长因子;内皮型一氧化氮合成酶
KEYWORDS: Alprostadil; Hypoxia-induced injury; Human pulmonary microvascular endothelial cells; Vascular endothelial growth factor; Endothelial nitric oxide synthase
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