摘要
目的探讨Toll样受体4（TLR4）在失血性休克并发急性肺损伤（Au）小鼠肺组织血红素加氧酶-1（HO-1）表达中的作用。方法采用小鼠失血性休克复苏模型，48只rILR4基因突变型小鼠C3H／HeJ和野生型小鼠C3H／HeN随机分为2组：①假手术组；②失血休克复苏组。分别于失血性休克复苏后6h、24h和48h取颈动脉血行血气分析，检测肺组织HO-1蛋白和mRNA的表达、肺组织IL-6含量及髓过氧化物酶（MPO）活性。采用方差分析进行数据统计。结果失血休克复苏后24hC3H／HeN和C3H／HeJ的肺组织中HO-1mRNA和蛋白含量的表达、IL-6含量、MPO活性与假手术组比较显著增加（P〈0．01或P〈0．05）；与C3H／HeN鼠比较，休克复苏后24hC3H／HeJ鼠的HO-1mRNA和蛋白含量、IL-6含量和MPO活性明显降低（P〈0．01或P〈0．05）。C3H／HeN鼠休克复苏后24h并发Au并且PaO2／FiO2〈300mmHg。结论rILR4受体激活在失血性休克致Au肺组织HO-1的表达中扮演重要角色。
Objective To investigate the role of Toll-like receptor4 TLR4 in HO-1 expression in acute lung injury induced by bemon＇hngic shock in mice. Method Forty-eight mice including C3H/HeN mice and C3H/ HeJ mice were randomly divided into sham group and hemorrhagic shock group. The mouse model of non-lethal hemorrhagic shock with resuscitation was used to observe the expression of HO- 1, the level of IL-6 in lung tissue homogenate and pulmonary myeloperoxidase （MPO） activity. Blood samples were assayed immediately after being taken from the carotid artery at 6 h, 24 h and 48 h after hemorrhagic shock. ANOVA were used to analyze the data. Results The expressions of HO-1 and the levels of IL-6 and MPO in lung tissue were higher 24 h hemorrhage than those in sham group （P〈0.01 or P〈0.05）; Compared with C3H/HeN mice, the expressions of HO-1, the levels of IL-6 and MPO in C3H/HeJ mice were obviously lower 24 h after Hemorrhage （ P 〈 0.01 or P 〈 0.05）. PaO2/FiO2 〈 300 mmHg and ALI hemorrhage alone by induced occurred 24 h after bemorrhagic shock in C3H/HeN mice. Conclusion TLR4 plays an important role in HO-1 expression during acute lung injury induced by hemorrhage shock.
出处
《中华急诊医学杂志》
CAS
CSCD
2008年第2期141-144,共4页
Chinese Journal of Emergency Medicine
基金
湖北省卫生厅科研基金（GX2C61）
