摘要
目的探讨单纯性失血性休克(无复苏)后肺组织TLR4表达变化及意义。方法C57BL/6小鼠随机分为失血性休克组、脂多糖(LPS)刺激组、假手术组。复制各组动物模型,在不同时间点取出肺组织,通过免疫组化方法,观察TLR4在肺组织的表达变化。结果在失血性休克和LPS刺激后肺部出现明显的中性粒细胞浸润、红细胞渗出。在失血性休克1、2及4 h后,肺巨噬细胞、肺泡上皮细胞及肺间质TLR4表达逐渐增加,6 h开始下降;而LPS刺激后1、2、4及6 h肺TLR4表达逐渐增加。假手术组未见TLR4表达。结论失血性休克后肺TLR4变化可能与急性肺损伤(ALI)的发生有关。失血性休克及LPS刺激后肺组织TLR4变化增强了机体的非特异性免疫能力,同时增加了宿主对随后各种刺激的易感性,过度表达的TLR4可能造成组织、器官结构和功能的损害。
Objective To investigate the change of TLR4 expression in mice lungs with hemorrhagic shock without resuscitation.Methods The C57BL/6 mice were randomly divided into three groups,ie,hemorrhagic shock, lipopolysaccharide （LPS）-challenged and shame control group. The kinetic expression of TLR4 in the lungs was observed by immunohistochemistry. Results Hemorrhagic shock and LPS-challenge induced lung neutrophil infiltration and erythrecyte effusion. TLR4 expression in the alveolar macrophages, epithelium and interstitium was gradually increased at 1 h,2 h,4 h,but decreased at 6h after hemorrhagic shock. However,TLR4 expression was continually increased at 1 h, 2 h, 4 h, 6 h after LPS stimulation. No expression of TLR4 was detected in the shame group. Conclusions The ＇alteration of TLR4 expression in hmgs is probably correlated with acute lung injury and might reinforce the host innate immune response. TLR4 expression predisposes the host to secondary insult after hemorrhagic shock and LPS stimulation. Over-expression of TLR4 may participate in tissues and organs structural and functional impairment.
出处
《中国呼吸与危重监护杂志》
CAS
2005年第6期435-437,i0001,共4页
Chinese Journal of Respiratory and Critical Care Medicine
关键词
失血性休克
TLR4
脂多糖
Hemorrhagic shock
TLR4
Lipopolysaccharide
