缺氧和IL-1β对人鼻黏膜上皮细胞环氧化酶-2表达和前列腺素E2释放的影响

Effect of hypoxia and IL-1β on COX-2 expression and PGE2 release in human nasal epithelia

目的:检测不同时间梯度的缺氧和(或)IL-1β诱导人鼻黏膜上皮细胞(HNE)环氧化酶-2(COX-2)表达和前列腺素E2(PGE2)释放状况,探讨其在鼻黏膜炎症发病机制中的作用。方法:应用Western Blot和荧光实时定量PCR技术检测缺氧和(或)IL-1β诱导后HNE中COX-2表达的变化。以酶标免疫测定检测PGE2的释放水平。均数间比较采用秩和检验,缺氧和IL-1β诱导间的交互作用分析采用广义线性模型。结果:COX-2和PGE2在正常HNE中呈微弱表达。缺氧和(或)IL-1β均呈时间依赖性诱导HNE中COX-2表达及PGE2释放,各时间点COX-2表达均较对照组明显增加(P<0.05)。其中,缺氧+IL-1β组诱导作用最强,缺氧组和IL-1β组依次减弱。缺氧+IL-1β组诱导的COX-2表达量及PGE2释放量高于同时间点缺氧组和IL-1β组分别诱导量之和。结论:缺氧和IL-1β均可有效诱导HNE中COX-2表达和PGE2释放,且缺氧和IL-1β具有协同诱导作用,提示COX-2参与了缺氧和IL-1β诱导的HNE体外炎症过程。

Objective：To detect cyclooxygenase-2 （COX-2） expression and prostaglandin E2 （PGE2） release in human nasal epithelia （HNE） induced by hypoxia and/or IL-1β of different time gradient, and to investigate their roles in nasal inflammatory pathogenesy. Method： Western Blot and fluorescent real time quantitative PCR were performed to detect the expression of COX-2 in HNE induced by hypoxia and/or IL-1β. The concentrations of PGE2 were determined by enzyme immunoassay. Median comparison was statistically treated by rank sum test, and generalized linear model was used to analyze the association of hypoxia with IL-1β. Result：Weak expressions of COX-2 and PGE2 were detected in normal HNE. COX-2 expression and PGE2 release increased in HNE induced by hypoxia and/or IL- 1β in time-dependent manner. Stronger expressions of COX-2 and PGE2 induced by hypoxia and/or IL-1β than control were detected on different time （P〈0.05）. The strongest inducible effect was found in hypoxia＋IL-1β group, and inducible effect decreased in hypoxia group and IL-1β group in turn. The expressions of COX-2 and PGE2 in hypoxia＋IL- 1β group were more than the sum of hypoxia group and IL-1β group on same time. Conclusion： Hypoxia and/or IL-1β effectively induce COX- 2 expression and PGE2 release in HNE. Synergistic effect between hypoxia and IL-1β has been found in induction of COX-2 and PGE2 in HNE. Results indicate that the increased expressions of COX -2 and PGE2 are involved in inflammation of HNE induced by hypoxia and/ or IL- 1β in vitro.