摘要
目的观察Toll样受体4（TLR4）对失血性休克小鼠所致急性肺损伤（ALI）中肺组织血红素加氧酶-1（HO-1）和诱导型一氧化氮合酶（iNOS）的影响。方法TLR4基因突变型小鼠C3H／HeJ和野生型小鼠C3H／HeN（48只），随机分为假手术组和失血性休克（6、24、48h）组。采用小鼠失血性休克致急性肺损伤模型，观察血气分析，HO-1和iNOS蛋白表达，白细胞介素-6（IL-6）水平，肺组织肺湿／干重比和病理形态学改变。结果与假手术组比较，C3H／HeN和C3H／HeJ小鼠失血休克后24h肺组织HO-1蛋白强阳性表达，IL-6含量明显增加为365．38±48，26和300．89±39．34；6h肺组织iNOS蛋白强阳性表达（P〈0．01）。与C3H／HeN小鼠比较，C3H／HeJ小鼠失血休克后24h肺组织HO-1、IL-6含量和W／D明显降低（P〈0．05）；6h肺组织iNOS蛋白显著减少为0．049±0．013。病理学检查显示失血休克后各时点肺组织损伤程度较假手术组明显加重。结论TLR4在失血性休克后ALI过程中被激活，通过影响HO-1和iNOS的表达参与了失血性休克致急性肺损伤的过程。
Objective To investigate the effect of TLR4 on HO-1 and iNOS protein expressions in acute lung injury induced by hemorrhagic shock in mice. Methods Forty eight C3H/HeJ （endotoxintolerant） mice and C3H/HeN （endotoxin-sensitive） mice were randomly divided into sham group and hemorrhagic shock （6h ,24h and 48h） group. A mouse model of non-lethai hemorrhagic shock and resuscitation was used to observe blood gas analysis, HO-1 and iNOS expressions,IL-6 level,wet/dry and the pulmonary pathologic changes. Results Compared with sham group,the expression of HO-1 and IL-6 level in lung tissue were markedly increased at 24h post-hemorrhagic shock （ 365.38 ± 48.26 and 300.89 ± 39. 34） ;The expressions of iNOS were increased at 6h post-hemorrhagic shock. Compared with C3H/HeN mice,HO-lexpression,IL-6 level and W/D in C3H/HeJ mice significantly decreased at 24h post-hemorrhagic shock （P 〈 0.05 ） ; The expression of iNOS of C3H/HeJ mice significantly decreased at 6h posthemorrhagic shock. （0. 049 ± 0. 013 ）. Under light microscope, the pathologic changes induced by hemorrhagic shock were significantly enhanced. Conclusion TLR4 was activated in the process of acute lung injury induced by hemorrhagic shock and HO-1 and iNOS are probably involved in the action mechanisms of ALI.
出处
《中华实验外科杂志》
CAS
CSCD
北大核心
2008年第9期1149-1151,共3页
Chinese Journal of Experimental Surgery
