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目的探讨慢性鼻-鼻窦炎(chronic rhinosinusitis,CRS)患者中鼻甲黏膜环氧合酶2(cyclooxygenase 2,COX-2)与丝裂原激活蛋白激酶(mitogen-activated protein kinase,MAPK)及核因子κB(nuclear factor kappa B,NF-κB)通路关键酶的表达及其相关性,明确其在黏膜炎性反应机制中的作用。方法将24例 CRS 患者中鼻甲外侧黏膜按海口分型分期标准分为3组(组1为Ⅰ型2期,组2为Ⅱ型2期,组3为Ⅲ型,每组8例),8例正常鼻黏膜作为对照。应用免疫组化和荧光实时定量多聚酶链反应检测 COX-2、p38丝裂原激活蛋白激酶(p38MAPK)、细胞外信号调节蛋白激酶(ERK)、c-Jun氨基端激酶(JNK)、NF-κB p65和 p50的表达,并分析其相关性。结果 COX-2、p38MAPK、ERK 和NF-κB在3组 CRS 中均有表达,强度高于对照组,差异有统计学意义(P 值均<0.05);3组 CRS 之间表达差异无统计学意义(P 值均>0.05);JNK 在 CRS 各组和对照组中均无阳性表达。相关性分析表明:CRS 各组中 COX-2、p38MAPK、ERK、NF-κB p65及 p50的蛋白质表达量同 mRNA 表达水平呈直线正相关(P 值均<0.05);在同一组 CRS 中 COX-2与 p38MAPK、ERK 的蛋白质和 mRNA 表达呈正相关(P 值均<0.05);CRS 各组中 COX-2表达与 NF-κB p65、p50的核内表达正相关(P<0.05)。结论CRS 中 COX-2表达上调,与上游 p38MAPK、ERK、NF-κB等信号转导通路具有相关性,提示 COX-2在CRS 鼻黏膜炎性反应中可能受后者调节。
Objective To investigate the relationship between cyclooxygenase 2 (COX-2) and mitogen-activated protein kinase (MAPK) and nuclear factor κB (NF-κB) in patients with chronic rhinosinusitis (CRS) (nuclear factor kappa B, NF-κB) pathway of key enzymes expression and its relevance to clarify its role in mucosal inflammatory response mechanism. Methods Twenty-four patients with CRS were divided into three groups according to the Haikou classification (group Ⅰ was type Ⅱ, group Ⅱ was type Ⅱ, group Ⅲ was type Ⅲ, and each group was 8) Normal nasal mucosa as a control. The expression of COX-2, p38 mitogen-activated protein kinase (p38MAPK), extracellular signal-regulated protein kinase (ERK), c-Jun N-terminal kinase (JNK) and NF- κB were detected by immunohistochemistry and real-time quantitative polymerase chain reaction p65 and p50 expression, and analyze their relevance. Results The expressions of COX-2, p38MAPK, ERK and NF-κB in CRS were higher than those in control group (P <0.05). There was no significant difference in CRS between the three groups Significance (P> 0.05). There was no positive expression of JNK in CRS and control groups. Correlation analysis showed that the expression of COX-2, p38MAPK, ERK, NF-κB p65 and p50 in each CRS group was positively correlated with the mRNA expression level (all P <0.05) 2 was positively correlated with the protein and mRNA expression of p38MAPK and ERK (all P <0.05). The expression of COX-2 in each group was positively correlated with the nuclear expression of p65 and p50 (P <0.05). Conclusions The up-regulation of COX-2 in CRS correlates with the upstream signal transduction pathway of p38MAPK, ERK and NF-κB, suggesting that COX-2 may be regulated by the latter in inflammatory reaction of CRS nasal mucosa.