摘要
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 significance of IκB kinase-β(IKK-β) and the protective effect of Ligustrazini(Lig) in acute lung injury(ALI) induced by hemorrhagic shock(HS) in rabbits. Methods Thirty rabbits were randomly divided into three groups: HS plus endotoxin group(n=10), Lig treatment group(n=10) and the normal group(n=10). In situ hybridization and immunohitochemistry combined with in situ quantitative analysis were used to detect the distribution and relative contents of IKK-β and NF-κB in lung tissues. The plasma concentration of tumor necrosis factor-α(TNF-α) was measured by ELISA. Morphological change of the lung was observed by light microscopy. Results Compared with the normal group, the expression levels of IKK-β(0.223±0.080), NF-κB(0.162±0.021), and TNF-α(809.33±201.6) were obviously increased in HS plus endotoxin group(P<0.05). Lig treatment could inhibit the expression of IKK-β(0.163±0.066) and NF-κB(0.120±0.020), decrease the plasma concentration of TNF-α(447.50±100.80)and alleviate the lung injury. Conclusion IKK-β/NF-κB/TNF-α may play a crucial role in the pathogenesis of ALI induced by HS. Lig could down-regulate the activity of IKK-β/ NF-κB pathway, and relieve HS-induced ALI.
出处
《中国医师杂志》
CAS
2005年第2期151-153,共3页
Journal of Chinese Physician
基金
国家自然科学基金资助项目 (30 0 0 0 1 65)