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目的:探讨NF-κB“诱饵”寡核苷酸对TNBS灌肠诱导BALB/C小鼠模型肠道炎症,NF-κB p65蛋白表达及TNF-α、IL-1β、TGF-βmRNA表达的影响,研究其对实验性结肠炎的治疗效果及机制。方法:将40只BALB/C小鼠随机分为正常对照组(NC组)、模型对照组(TNBS组)、NF-κB p65错义寡核苷酸组(MSODN组)和NF-κB“诱饵”寡核苷酸组(Decoy ODN组),采用2,4,6-三硝基苯磺酸(TNBS)灌肠造模。造模24 h后对各组进行相应灌肠治疗,光镜下观察肠黏膜炎症并评分,免疫组化检测各组小鼠肠黏膜NF-κB p65蛋白表达,逆转录聚合酶链反应(RT-PCR)检测各组小鼠结肠组织TNF-α、IL-1β、TGF-βmRNA表达。结果:Decoy ODN组小鼠在结肠炎症评分较TNBS组和MSODN组明显改善(P<0.05)。Decoy ODN组小鼠肠黏膜NF-κB p65蛋白表达与NC组和MSODN组比较无明显差异(P>0.05)。Decoy ODN组小鼠结肠组织TNF-α、IL-1β、TGF-βmRNA的表达水平较TNBS组和MSODN组明显减少(P<0.05)。结论 :NF-κB Decoy ODN对小鼠TNBS结肠炎有较好的治疗作用,其作用机制可能是通过下调炎性因子TNF-α、IL-1β、TGF-β的表达实现的。
OBJECTIVE: To investigate the effect of NF-κB decoy on intestinal inflammation, the expression of NF-κB p65 and the expression of TNF-α, IL-1β and TGF-βmRNA in BALB / c mouse model induced by TNBS , To study its therapeutic effect on experimental colitis and mechanism. Methods: 40 BALB / C mice were randomly divided into normal control group (NC group), model control group (TNBS group), NF-κB p65 missense oligonucleotide group (MSODN group) and NF- Decoy ODN group ", using 2,4,6-trinitrobenzene sulfonic acid (TNBS) enema. The rats in each group were subjected to the corresponding enema treatment 24 hours after the model was established. The inflammation of the intestinal mucosa was observed under the light microscope and scored. The expression of NF-κB p65 protein in the intestinal mucosa was detected by immunohistochemistry and the expression of NF- ) Were used to detect the expression of TNF-α, IL-1β and TGF-βmRNA in colonic tissue of mice in each group. Results: The Decoy ODN mice in the colon inflammation score than TNBS group and MSODN group was significantly improved (P <0.05). The expression of NF-κB p65 protein in intestinal mucosa of Decoy ODN group had no significant difference compared with NC group and MSODN group (P> 0.05). The expression of TNF-α, IL-1β and TGF-βmRNA in the colon tissues of Decoy ODN group was significantly lower than that of TNBS group and MSODN group (P <0.05). CONCLUSION: NF-κB Decoy ODN has a good therapeutic effect on TNBS colitis in mice. The mechanism may be through down-regulating the expression of inflammatory cytokines TNF-α, IL-1β and TGF-β.