摘要
目的:探讨Toll样受体4(TLR4)突变在单纯性失血性休克(无复苏)所致小鼠急性肺损伤(ALI)中的作用及机制。方法:以TLR4基因突变的C3H/HeJ品系及TLR4野生型的CBA品系小鼠为研究对象,每组20只。心脏穿刺复制失血性休克模型,在不同时间点取出肺组织,观察肺组织病理形态变化;通过逆转录-聚合酶链反应(RT-PCR)半定量方法检测肺组织TLR4 mRNA的表达水平;用凝胶电泳迁移(EMSA)法检测肺组织中核因子-κB(NF-κB)的量。结果:失血性休克刺激后,基因突变小鼠肺组织中性粒细胞浸润、红细胞渗出较野生型小鼠明显减轻;基因突变小鼠肺组织TLR4 mRNA表达及NF-κB活性变化不明显,而野生型小鼠TLR4 mRNA在2、4和6h表达增加,NF-κB在失血性休克后1和2 h活性显著增加。结论:TLR4在失血性休克所致ALI中起重要作用,其突变可减轻失血性休克所致的ALI。
Objective ：To investigate the role and its mechanism of Toll-like receptor4 （TLR4） mutation on acute lung injury induced by hemorrhagic shock without resuscitation. Methods：The hemorrhagic shock model of 20 toll-like receptor 4 （TLR4） mutant mice and 20 wild type mice （CBA） was reproduced by heart puncture. The lung tissues were collected at 0,1, 2, 4 , and 6 hours after hemorrhagic shock for pathologic analysis, TLR4 mRNA was measured by semi-quantitative reverse transcription-polymerase chain reaction and NF-KB activation was determined by electrophoretic mobility shift assay. Results：The lung neutrophil infiltration and erythrocyte effusion in toll-like receptor 4 mutant mice were milder than those in wild type mice. The expression of TLR4 mRNA and activation of NF-kB were increased following hemorrhagic shock in wild type mice, while there was no significant change in TLR4 mutant mice. Conclusion：TLR4 plays an important role in ALI induced by hemorrhagic shock, and TLR4 mutant alleviates ALI.
出处
《医学研究生学报》
CAS
2007年第5期494-497,I0004,共5页
Journal of Medical Postgraduates
基金
江苏省自然科学基金资助项目(批准号:BK2004096)
