王肖, 尹文, 黄杨, 史小鹏, 杨天伦, 周知, 李传昶. 血管紧张素Ⅱ诱导内皮细胞产生IL-8和Duffy抗原/趋化因子受体的研究[J]. 心脏杂志, 2011, 23(2): 173-176.
    引用本文: 王肖, 尹文, 黄杨, 史小鹏, 杨天伦, 周知, 李传昶. 血管紧张素Ⅱ诱导内皮细胞产生IL-8和Duffy抗原/趋化因子受体的研究[J]. 心脏杂志, 2011, 23(2): 173-176.
    Angiotensin II stimulates production of interleukin-8 and Duffy antigen/receptor for chemokine from endothelial cells[J]. Chinese Heart Journal, 2011, 23(2): 173-176.
    Citation: Angiotensin II stimulates production of interleukin-8 and Duffy antigen/receptor for chemokine from endothelial cells[J]. Chinese Heart Journal, 2011, 23(2): 173-176.

    血管紧张素Ⅱ诱导内皮细胞产生IL-8和Duffy抗原/趋化因子受体的研究

    Angiotensin II stimulates production of interleukin-8 and Duffy antigen/receptor for chemokine from endothelial cells

    • 摘要: 目的: 探讨Duffy抗原/趋化因子受体(DARC)和IL-8在血管紧张素Ⅱ(AngⅡ)致炎机制中可能的作用。方法: 体外培养人脐静脉内皮细胞,分别用PBS(对照组)、AngⅡ(10-7 mol/L)诱导0~24 h,收集0、6、12、24 h4个时间点的细胞培养上清和内皮细胞,采用ELISA法分别检测细胞培养上清和内皮细胞裂解液中IL-8的水平;采用实时定量PCR检测内皮细胞中DARC mRNA的表达。结果: AngⅡ(10-7 mol/L)能诱导内皮细胞产生并释放IL-8,且存在时间依赖性。细胞培养上清中IL-8的水平6~12 h内逐渐增高,24 h后则降低;细胞裂解液中IL-8水平的变化也存在时间依赖性,6~24 h内逐渐增高,其变化与细胞培养上清不平行。AngⅡ可诱导内皮细胞中DARC mRNA表达,也存在时间依赖性,6~24 h逐渐增高。结论: AngⅡ能诱导人内皮细胞产生并释放IL-8和表达DARC。内皮细胞DARC可能通过结合固定IL-8促进趋化因子浓度梯度的形成而参与炎症反应过程。

       

      Abstract: AIM: To explore the roles of interleukin-8 (IL-8) and Duffy antigen/receptor for chemokine (DARC) in AngII-induced inflammation in endothelial cells. METHODS: Endothelial cells from human umbilical vein (HUVEC) were cultured and stimulated with Ang II (10-7 mol/L) for 0-24 h with phosphate-buffered saline (PBS)as the control. The supernatant and cell lyses of endothelial cells were collected at 0, 6, 12 and 24 h. IL-8 levels were measured by enzyme-linked immunosorbent assay (ELISA). DARC mRNA expression in endothelial cells was measured by real-time polymerase chain reaction (real-time PCR). RESULTS: AngII(10-7mol/L)stimulated IL-8 production in a time-dependent manner. IL-8 level in the supernatant increased gradually during 0-6 h and decreased at 24 h. IL-8 level in cell lyses also increased during 6-24 h in a time-dependent manner, but the changes were not parallel with those in the supernatant. Ang II also stimulated DARC mRNA expression during 6-24 h in a time-dependent manner. CONCLUSION: AngII stimulates IL-8 release and DARC expression from HUVECs. IL-8 and DARC may be involved in the process of AngII-induced inflammation, suggesting that DARC binds IL-8 to form chemokine concentration gradient in inflammation.

       

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