摘要
目的探讨热休克蛋白70(HSP70)对严重创伤休克后肝脏作用。方法成年Wistar大鼠,采用双侧股骨骨折伴失血性休克致严重创伤模型,动态观察伤后8h大鼠肝组织HSP70、血清肝功能生化指标、肝脏病理等变化。HSP70表达测定采用免疫印迹法,并进行计算机图像分析。结果伤后HSP70在肝组织中表达迅速增加,6h达到峰值,伤后8h仍维持较高水平;创伤合并休克后,HSP70表达高峰提前至伤后4h,持续表达至伤后6h后逐渐下降,死亡前在肝组织中仍有少量表达。创伤休克后血清ALT、TB伤后4h开始明显增高(P<0.01),白蛋白下降(P<0.01)。肝脏镜下创伤休克后6h肝窦内出现较多炎性细胞浸润。结论在创伤休克早期,HSP70可能参与了肝组织细胞抗损伤机制的启动,但随着休克时间的延长,HSP70的过高持续表达,则可能对肝脏造成损害。HSP70在创伤休克后肝保护与肝损害过程中可能发挥双重作用。
Objective To study the effect of heat shock protein 70 （HSP70） on liver protection and damage in hemorrhagic shock after trauma. Methods Hemorrhagic shock with bilateral femur fracture models were produced in adult wistar rats. Changes of hepatic tissue HSP70, liver pathology, hepatic function markers in serum were dynamically observed. The expression of HSP70 in hepatic tissue was assayed by western blot, and analyzed with computer imaging system. Results HSP70 was gradually increased in hepatic tissue after severe trauma, increased to the highest at 6 hours after trauma, and still maintained at a high level at 8 hours after trauma. But hepatic function markers and pathology didn＇t change obviously after trauma. After trauma with hemorrhagic shock, HSP70 was much more strengthened than simple trauma group, reached its peak at 4 to 6 hours after trauma, and low expression still existed before death. ALT and TB in serum were increased obviously at 4 hours after trauma （ P 〈 0.01 ）, albumin was obviously decreased （ P 〈 0.01 ） . There were more inflammatory cells intiltrated in hepatic sinusoid at 6 hours after trauma. Conclusion HSP70 may participate in anti-injury mechanism of hepatic tissue cell, but excessive expression of HSP70 may cause injury to liver during hemorrhagic shock after trauma. HSP70 may have functions of protection and damage in liver during hemorrhagic shock after trauma.
出处
《中华急诊医学杂志》
CAS
CSCD
2005年第11期907-909,共3页
Chinese Journal of Emergency Medicine
基金
重庆市自然科学基金资助项目(2004-BB5068)
国家重点基础研究发展规划资助项目(G1999054200)
