摘要
目的研究信号转导和转录激活因子6(STAT6)与核因子(NF)-κB在实验性结肠炎大鼠中的表达。方法 18只SD雄性大鼠随机分为3组:正常对照组、模型组、美沙拉嗪组,每组6只。模型组和美沙拉嗪组大鼠均采用三硝基苯磺酸(TNBS)造模。模型组不设干预,正常饮食;美沙拉嗪组给予美沙拉嗪混悬液灌胃;治疗15d后观察大鼠的结肠病理组织学改变,用RT-PCR法检测大鼠结肠组织STAT6mRNA的表达,并用Western Blot法检测大鼠脾淋巴细胞NF-κBp65的表达。结果 STAT6 mRNA在溃疡性结肠炎组织中的表达明显高于正常结肠组织(P<0.01);大鼠脾淋巴细胞NF-κBp65蛋白在模型组的表达也明显高于正常组(P<0.01);与模型组相比,美沙拉嗪组STAT6 mRNA和NF-κBp65的表达明显下降(P<0.01)。结论 STAT6 mRNA和NF-κB p65在实验性结肠炎大鼠中呈现高表达。美沙拉嗪可能是通过STAT6和NF-κB双信号途径下调炎症,从而发挥治疗作用。
Objective To evaluate the expression of signal transducer and activator of transcription 6 （STAT6） and nuclear factor-κB （NF-κB） in rats with experimental ulcerative colitis （UC）. Methods 18 male rats were randomly assigned to the following groups （n = 6）： control group, model group, mesalazine group. The rats were induced by trinitrobenzene sulfonic acid （TNBS） in model group and mesalazJne group. The rats in mesalazine group were given mesalazine through intragastrie administration for 15 days. Colonic histopalhologic changes were observed. The expression of STAT6 mRNA of UC tissue was detected by RT PCR, and the protein expression of NF-κB p65 was analyzed by western blot method. Results Compared with the control group, there was elevated expression of STAT6 mRNA and NF-κB p65（P〈0.01 ） in rats with experimental UC. After UC model treated with mesalazine, the level of STAT6 mRNA and NF-κB p65 was significantly decreased （P〈0. 01） in mesalazine group. Conelusions High expression of STAT6 mRNA and NF-κB p65 in rats with experimental ulcerative colitis, and regulating the expression of STAT6 and NF-κB double signal transduction pathway may be the anti-inflammatory mechanism of mesalazine.
出处
《国际消化病杂志》
CAS
2010年第5期311-313,共3页
International Journal of Digestive Diseases
基金
国家自然科学基金项目(30772878)
