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目的 探讨IκB激酶 -β(IKK -β)在失血性休克继发急性肺损伤中的意义及川芎嗪 (Ligustrazini ,Lig)的调节干预作用。方法 采用原位杂交、免疫组织化学结合原位定量分析以及酶联免疫吸附试验分别检测模型组、川芎嗪组、对照组肺组织IKK -β、核因子 (NF) -κB表达以及血浆肿瘤坏死因子 -α(TNF -α)含量 ,并行病理学光镜检查。结果 模型组上述指标依次为 [(0 2 2 3±0 0 80 )、(0 162± 0 0 2 1)、(80 9 3 3± 2 0 1 6)ng/L] ,较对照组升高 (P <0 0 5 ) ,肺组织有明显炎症改变 ,川芎嗪组上述指标依次为[(0 163± 0 0 66)、(0 12 0± 0 0 2 0 )、(4 4 7 5 0± 10 0 80 )ng/L] ,较模型组降低 (P <0 0 5 ) ,肺组织炎症改变减轻。结论 IKK -β/NF -κB/TNF -α效应是失血性休克继发急性肺损伤的重要机制 ;川芎嗪可下调IKK -β/NF -κB通路减轻失血性休克后的急性肺损伤。
Objective To investigate the role of IκB kinase-β (IKK-β) in acute lung injury secondary to hemorrhagic shock and the regulatory intervention of Ligustrazini (Lig). Methods In situ hybridization, immunohistochemistry combined with in situ quantitative analysis and enzyme-linked immunosorbent assay were used to detect the expression of IKK-β, NF-κB and plasma tumor necrosis factor in lung tissue of model group, tetramethylpyrazine group and control group. -α (TNF-α) content, parallel pathology light microscopy. Results The above indicators in the model group were [(0232 ± 0 0 80), (0 162 ± 0 0 21), (80 9 3 3 ± 2 0 16) ng/L], which was higher than the control group. (P <0 05), there was a significant change in inflammation in lung tissue. The above indicators in the ligustrazine group were [(0 163 ± 0 0 66), (0 12 0 ± 0 0 2 0), (4 4 7 0 0 ± 10 0 80 ng/L] was lower than that in the model group (P <0 05), and the inflammation in the lung tissue was reduced. Conclusion The effect of IKK-β/NF-κB/TNF-α is an important mechanism of acute lung injury secondary to hemorrhagic shock. Ligustrazine can down-regulate IKK-β/NF-κB pathway in acute lung injury after hemorrhagic shock.