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目的探讨NF-κB通路在大鼠急性结肠炎应激反应中的作用。方法建立大鼠急性结肠炎应激模型,固定化蛋白印迹法(Western blot)检测脊髓内I-κB蛋白水平,逆转录-聚合酶链式反应法(RT-PCR)检测脊髓内COX-2 mRNA水平,免疫组化法检测L5-S1和C2-4脊髓内COX-2蛋白水平。结果结肠内灌注6％醋酸可产生明显局部炎症反应;急性结肠炎0．5 h后L5-S1脊髓内I-κB 蛋白表达明显上调(P<0．05);急性结肠炎3 h后I5-S1脊髓内COX-2 mRNA表达开始增加,24 h后达到高峰;免疫组化结果显示结肠炎24 h后胞浆内COX-2蛋白表达增加。结论大鼠急性结肠炎时,NF-κB通路可能通过调控COX-2的表达而介导炎症反应,I-κB有可能成为急性结肠炎治疗的靶点。
Objective To investigate the role of NF-κB pathway in the stress response of acute colitis in rats. Methods The rat model of acute colitis was established. The level of I-κB protein in the spinal cord was detected by Western blot and the expression of COX-2 mRNA in the spinal cord was detected by reverse transcription-polymerase chain reaction (RT-PCR) The levels of COX-2 protein in the spinal cord of L5-S1 and C2-4 were detected by immunohistochemistry. Results The intracolonic perfusion of 6% acetic acid produced obvious local inflammatory response. The expression of I-κB protein in L5-S1 spinal cord was significantly increased after 0.5 h of acute colitis (P <0.05) The expression of COX-2 mRNA in S1 spinal cord began to increase and peaked 24 hours later. The expression of COX-2 protein in cytoplasm increased after 24 hours in colitis. Conclusion NF-κB pathway may mediate inflammatory response by regulating the expression of COX-2 in acute colitis, and I-κB may be the target of acute colitis treatment.