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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。
AIM: To investigate the effect of lipopolysaccharide (LPS) on the expression of hypoxia inducible factor-1α (HIF-1α) in murine peritoneal macrophages in vitro and its possible mechanism. Methods: Peritoneal macrophages of BALB / c mice were treated with LPS alone or in combination with sulfapyridine and the inhibitor of nitric oxide synthase (L-NMMA), respectively. PCR was used to detect the changes of HIF-1αmRNA. The changes of HIF-1αprotein and vascular endothelial growth factor (VEGF) protein were detected by immunocytochemistry. Results: After treated with LPS for 10h, there was no significant change in HIF-1αmRNA, HIF-1αprotein and VEGF protein (P <0.01), NF-κB inhibitor sulfasalazine and nitric oxide synthase Inhibitor L-NMMA could reduce the induction of HIF-1α protein and VEGF protein by LPS (P <0.05). Conclusion: LPS can up-regulate the expression of HIF-1α by post-transcriptional pathway. The expression of HIF-1α protein can further induce the expression of VEGF in its target gene.