Toll样受体4介导炎症及凋亡信号通路在新生儿小肠结肠炎动物模型中的作用探讨

摘要

Objective To investigate the effects of TLR4-mediated inflammation and apoptotic signaling path-ways on neonatal necrotizing enterocolitis (NEC) and intestinal cell apoptosis. Methods The NEC animal models were established in neonatal TLR4-deficient mice and matched TLR4-wild type mice and induced by multiple factors. The mRNA expression of TLR4, ReLA/p65, caspases 8, caspase 9 and caspase3 were determined by RT-PCR. The changes in the levels of intestinal cell apoptosis were determined. Results There were significantly changes in the levels of cell apoptosisafter the NEC animal models were successfully induced. The ReLA/p65 and Caspase 8 expres-sion were decreased and the Caspase 9 expression was increased in the TLR4-deficient group. The ReLA/p65 and Caspase 8 expression were increased and the Caspase 9 expression was decreased in the TLR4-wild type group. Con-clusion TLR4-mediated inflammation-apoptotic signaling pathway may inhibit the cell apotosis in the course of NEC.%目的：探讨Toll样受体（TLR）4炎症及凋亡信号通路对于新生儿坏死性小肠结肠炎（NEC）炎症及肠道细胞凋亡的影响。方法通过多因素联合作用对新生TLR4基因缺失小鼠和相应野生型小鼠进行诱导NEC动物模型。采用实时荧光定量聚合酶链反应（RTPCR）检测肠组织TLR4、ReLA/p65、胱天蛋白酶（caspases）8， caspase 9，caspase3的mRNA表达，并检测肠道细胞的凋亡水平变化。结果被成功诱导NEC后细胞凋亡水平有明显变化，缺失株处理组ReLA/p65与Caspase 8表达下降，Caspase 9表达上调，野生株处理组ReLA/p65与Caspase 8表达上调，Caspase 9表达下降。结论 TLR4介导的炎症-凋亡信号通路对NEC病程中的细胞凋亡起到了抑制作用。