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机构地区:[1]苏州大学医学部病理生理学教研室,江苏苏州215123 [2]江苏省无锡市人民医院中心实验室,江苏无锡214023
出 处:《吉林医学》2009年第19期2232-2235,共4页Jilin Medical Journal
摘 要:目的:探讨在体外常氧环境下脂多糖(LPS)对小鼠腹腔巨噬细胞缺氧诱导因子-1α(HIF-1α)表达的影响及其可能的机制。方法:分别以LPS单独或联合NF-κB抑制剂柳氮磺胺吡啶、一氧化氮合酶抑制剂L-NMMA作用于BALB/c小鼠腹腔巨噬细胞,用逆转录聚合酶链反应(RT-PCR)法检测HIF-1αmRNA的变化,用免疫细胞化学法检测HIF-1α蛋白和血管内皮生长因子蛋白(VEGF)的变化。结果:LPS作用于小鼠巨噬细胞10h后,HIF-1αmRNA无明显变化,HIF-1α蛋白和VEGF蛋白明显增加(P<0.01),NF-κB抑制剂柳氮磺胺吡啶和一氧化氮合酶抑制剂L-NMMA均可降低LPS对HIF-1α蛋白和VEGF蛋白表达的诱导作用(P<0.05)。结论:LPS可通过转录后途径上调HIF-1α的表达,HIF-1α蛋白的表达又可进一步诱导其靶基因VEGF的表达。Objective To investigate the effect of LPS on HIF - 1α expression in murine peritoneal maerophages and its possible mechanism. Method The peritoneal macrophages from BALB/c mice were collected and treated with LPS combined with or without NF - κB inhibitor SSZ or NOS inhibitor L - NMMA. The level of HIF - 1α mRNA was measured by RT - PCR. The expression of HIF - 1α & VEGF protein was determined by immunocytoehemistry. Results After the peritoneal maerophages being treated with LPS for 10h, the level of HIF -1α mRNA had no significant changes than that of the control group,and the expression of HIF -1α & VEGF protein was significantly higher than that of the control group (P 〈 0. 01 ). Moreover, SSZ and L - NMMA could attenuate the expression of HIF - 1α & VEGF protein induced by LPS ( P 〈 0. 05 ). Conclusion LPS can up - regulate the expression of HIF - 1α and its target gene VEGF by post - transcription mechanism.
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