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目的 探讨IκB激酶 - β(IKK - β)在失血性休克继发肝脏损伤中的作用。 方法 采用失血性休克家兔模型 ;分离培养肝脏枯否氏细胞 (KC) ,用原位杂交方法 (ISH)、凝胶电泳迁移率改变分析法 (EMSA)和酶联免疫吸附实验 (ELISA)分别检测KC中IKK - βmRNA表达、核因子 (NF) -κB活性和KC培养液上清中TNF -α含量。并进行肝脏组织的病理学光镜检查。结果 模型组KC中IKK - β的mRNA表达 (0 1 7± 0 0 4 )、NF -κB活性 (1 72± 0 36 )和培养液上清中TNF -α含量 (30 0 0 5± 30 86 )ng/L较对照组 [IKK - β(0 0 2± 0 0 1 )、NF -κB(0 31± 0 1 0 )、TNF -α(1 34 85± 1 2 0 9)ng/L]明显增高 (P均 <0 0 1 )。模型组肝脏组织病理损伤严重。结论 IKK - β介导NF -κB活化诱发细胞因子释放在失血性休克诱发肝脏损害的病理机制中发挥重要作用
Objective To investigate the role of IκB kinase - β (IKK - β) in hepatic injury secondary to hemorrhagic shock. Methods Hemorrhagic shock model was established in rabbits. Kupffer cells (KCs) were isolated and cultured in situ hybridization (ISH), electrophoretic mobility shift assay (EMSA) and enzyme-linked immunosorbent assay (ELISA) The expression of IKK - βmRNA, the activity of nuclear factor (NF) - κB and the level of TNF - α in the supernatant of KC culture medium were detected. Liver pathology and light microscopy. Results The mRNA expression of IKK - β (0 1 7 ± 0 0 4), NF - κB activity (1 72 ± 0 36) and TNF - α in the supernatant of the culture medium in the model group (30 000 ± 30 86 ) ng / L was significantly higher than that of the control group [IKK - β (0 0 2 ± 0 0 1), NF - κB 0 31 ± 0 1 0, TNF - α 1 34 85 ± 1 2 0 9] ng / L] Was significantly higher (P <0.01). The model group of liver tissue pathological damage. Conclusion IKK - β plays an important role in the pathological mechanism of liver damage induced by hemorrhagic shock induced by the release of cytokines induced by NF - κB activation