核因子-κB和激活蛋白-1在恶唑酮诱导的小鼠实验性肠炎中的表达

目的 研究恶唑酮诱导的小鼠实验性肠炎中核因子(NF)-κB和激活蛋白(AP)-1基因表达量的变化,以探索其在发病机制中的意义.方法 7～8周龄的健康昆明小鼠24只,体重25～30 g,均分为正常组和模型组.模型组小鼠采用3%恶唑酮皮肤致敏5 d后,以0.5%恶唑酮(溶解于50%乙醇中)0.15 ml一次性灌肠造模方式建立实验性结肠炎模型.3 d后处死所有小鼠,分别提取外周血单个核细胞(PBMC)、脾脏单个核细胞(SMC)和肠黏膜固有层单个核细胞(LPMC).经细胞mRNA抽提、逆转录cDNA后进行荧光定量PCR(Taqman探针法)检测NF-κB、AP-1的表达量.并进行结肠炎的组织学评分.结果 模型组NF-κB在SMC、LPMC和PBMC中的表达量均比正常组明显增高(分别为5.62±0.78比3.16±0.59、5.46±0.38比3.18±0.58、5.65±0.56比3.36±0.59,P＜0.01),AP-1亦是如此(分别为5.61±0.54比3.22±0.50、5.50±0.69比3.19±0.40、5.67±0.44比3.27±0.41,P＜0.01).结论 NF-κB、AP-1的活化可能与结肠炎的发病机制有关.

The expressions of nuclear factor-κB and activator protein-1 in oxazolone induced colitis in mice

Objective To investigate the expression changes of nuclear factor(NF)-κB and activator protein (AP)-1 in oxazolone induced colitis in mice and their mechanisms. Methods Twenty-four mice were randomly divided into normal group and model group with 12 each. Experimental colitis was induced with skin sensitization of 3% oxazolone for 5 days, then rectal administration of 0.15 ml of 0. 5% oxazolone solution in mice. All mice were sacrificed on day 3. Peripheral blood mononuclear cells (PBMC), spleen mononuclear cells (SMC) and lamina propria mononuclear cells (LPMC) were isolated from the colon tissues. Expression of NF-κB and AP-1 in SMC, LPMC and PBMC were determined by fluorescence quantitative polymerase chain reaction (PCR). The colitis was evaluated histologically. Results The expressions of NF-κB and AP-1 in SMC, LPMC,PBMC of model groupwere significantly higher than those in normal group(NF-κB : 5.62±0.78 vs. 3.16±0.59,5.46±0.38 vs. 3.18±0.58, 5.65±0.56 vs. 3.36±0.59, P＜0.01; AP-1; 5.61±0.54 vs. 3.22±0.50, 5.50±0.69 vs. 3.19± 0.40,5.67±0.44 vs. 3. 27±0.41, P＜0.01). Conclusion The activation of NF-κB and AP-1 are involved in the mechanisms of ulcerative colitis.