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目的探讨Toll样受体4(TLR4)在老龄大鼠感染性多器官损伤发病中的意义。方法将大鼠分为老龄对照组、老龄模型组和青年对照组、青年模型组;选用气管插管法注入肺炎克雷伯杆菌,由肺炎导致多器官损伤;采用免疫组织化学和分子生物学技术,观察肺、心、小肠组织TLR4样受体信号转导通路主要相关分子表达变化。结果老龄模型组和青年模型组肺、心、小肠组织内毒素结合蛋白(LBP)、CD14、TLR4、白介素-1受体相关激酶(IRAK)mRNA和TLR4、肿瘤坏死因子受体相关因子-6(TRAF-6)、核因子-kB(NF-κB)阳性细胞数和/或光密度表达分别较老龄对照组和青年对照组明显增强(P<0.01或P<0.05),老龄模型组肺、心、小肠组织TLR4和NF-κB分子表达又较青年模型组增高显著(P<0.01或P<0.05)。结论 TLR4信号转导介导了老年感染性多器官损伤,并发挥了重要作用。
Objective To investigate the significance of Toll-like receptor 4 (TLR4) in the pathogenesis of infectious multiple organ injury in aged rats. Methods The rats were divided into the old control group, the aged model group, the young control group and the young model group. The rats were infused with Klebsiella pneumoniae by tracheal intubation and multiple organ injury was induced by pneumonia. Immunohistochemistry and molecular biology techniques , Observe the changes of TLR4-like signal transduction pathway-related molecules in lung, heart and small intestine. Results The expressions of endotoxin binding protein (LBP), CD14, TLR4, interleukin-1 receptor related kinase (IRAK) mRNA and TLR4 in lung, heart and small intestine of aged model group and young model group TRAF-6, NF-κB positive cells and / or optical density were significantly increased (P <0.01 or P <0.05) compared with the control group and the young control group , While the expressions of TLR4 and NF-κB in small intestine increased significantly (P <0.01 or P <0.05) than those in young model group. Conclusion TLR4 signaling plays an important role in the pathogenesis of senile infectious multiple organ injury.