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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 the expression of cyclooxygenase-2 (COX-2) and prostaglandin E2 (PGE2) in human nasal epithelial cells (HNE) induced by hypoxia and / or IL- The role of nasal mucosal inflammation in the pathogenesis. Methods: The changes of COX-2 expression in HNE induced by hypoxia and / or IL-1β were detected by Western Blot and real-time PCR. Enzyme immunoassay was used to detect the release of PGE2. The rank sum test was used to compare the mean and the generalized linear model was used to analyze the interaction between hypoxia and IL-1β induction. Results: COX-2 and PGE2 were weakly expressed in normal HNE. Hypoxia and / or IL-1βinduced COX-2 expression and PGE2 release in HNE in a time-dependent manner, and the expression of COX-2 at each time point was significantly higher than that in control group (P <0.05). Among them, hypoxia + IL-1βgroup had the strongest inducing effect, while the hypoxia group and IL-1βgroup decreased in turn. The COX-2 expression and PGE2 release induced by hypoxia + IL-1βgroup were higher than those induced by hypoxia and IL-1β at the same time. CONCLUSION: Both hypoxia and IL-1β can effectively induce COX-2 expression and release of PGE2 in HNE, and synergistic induction of hypoxia and IL-1β suggest that COX-2 is involved in the hypoxia and IL-1β induced HNE in vitro Inflammation process.