糖皮质激素受体在创伤失血性休克大鼠肝损伤中的作用  

The role of glucocorticoid receptor in hepatic injury after trauma with hemorrhagic shock in rats

作　　者：罗东林　[1] 刘宝华　[1] 周继红[1] 熊仁平[1] 李涛[2] 叶秀峰[1] 陈金萍[1] 

机构地区：[1]第三军医大学大坪医院野战外科研究所普外科,重庆400042 [2]重庆医科大学病理教研室,重庆400016

出　　处：《内分泌外科杂志》2007年第3期151-153,共3页

基　　金：国家重点基础研究发展规划资助项目（No：G1999054200）;重庆市自然科学基金项目（No：2004-BB5068）

摘　　要：目的从组织受体水平探讨糖皮质激素受体（GR）在创伤失血性休克后肝组织中的变化及其对肝损伤的作用机制。方法采用双侧股骨骨折伴失血性休克模型，并对GR进行阻断后再致伤，动态观察伤后8h大鼠肝组织GR、肝脏病理、肝功能生化指标、伤后8h大鼠死亡率等变化。肝组织GR采用免疫印迹法测定其蛋白含量，并进行计算机图像分析。结果肝组织GR的蛋白含量在创伤失血性休克后1h即开始下降，2h明显低于正常对照组（P〈0．01），6h降至最低，8h仍显著低于正常；光镜下伤后4h一8h肝窦内少许淤血，有散在炎性细胞浸润；血清丙氨酸氨基转移酶（ALT）、总胆红素（TB）伤后4h开始增高，白蛋白下降；大鼠死亡率10％。GR阻断后再致双侧股骨骨折并失血性休克，光镜下伤后2h肝窦内即可见较多炎性细胞浸润，血清ALT、TB在伤后2h即有明显升高（P〈0．01），白蛋白明显下降（P〈0．01）；大鼠死亡率明显升高（50％）。结论GR不足可导致严重创伤并失血性休克后肝损伤的发生；且减少越多，肝损害越重，死亡率越高。提示GR在严重创伤休克后肝组织细胞损伤与抗损伤机制方面可能起着重要作用。Objective To investigate changes and functions of GR at the level of tissue cell receptor in liver injury after trauma with hemorrhagic shock. Methods Adult Wistar rats were used and rats model was produced by adopting hemorrhagic shock in accompany with bilateral femur fracture. The changes of hepatic tissue GR, pathology of liver, hepatic function markers, and mortality were dynamically observed at lh-8h after trauma, and blocking GR before trauma with hemorrhagic shock. The expression of GR in hepatic tissue was assayed by western blot and then analyzed with computer imaging system. Results Protein content of GR in hepatic tissue after trauma, was obviously lower than normal at 2h after trauma（P〈0.01）, reduced to the lowest at 6h after trauma. Hepatic congestion was minimal, and there were little inflammatory cells infiltrped in hepatic sinusoid at 4h- 8h after trauma with hemorrhagic shock. Alanine aminotransferase（ALT） and Total bilirubin（TB） increased as well as albumin decreased at 4h after trauma. Mortality of 8h after trauma was 10%. After usage of GR blocking agent, there were much inflammatory cells infiltrated in hepatic sinusoid at 2h after trauma with hemorrhagic shock. Mortality after trauma 8h was 50%. Conclusions GR insufficiency might cause hepatic injury after trauma with hemorrhagic shock. The decreesed insufficiency is related with severe liver injury and higher mortality. It is indicated that GR act as an important role in injury and anti-injury mechanism of hepatic tissue＇ cell in secondary hepatic injury after trauma with hemorrhagic shock.

关 键 词：创伤 失血性休克 糖皮质激素受体 肝损伤 

分 类 号：R6[医药卫生—外科学]