摘要
目的 探讨严重创伤后糖皮质激素 (GC)、糖皮质激素受体 (GR)、热休克蛋白 (HSP70 )在肝脏继发性损伤中的作用机制。方法 成年雄性Wistar大鼠 88只 ,随机分成正常对照组、严重创伤组、阻断 5 0 %GR伴严重创伤组。采用严重胸部撞击伤伴单侧股骨骨折模型、动态观察创伤后大鼠血清皮质醇浓度、肝组织GR及HSP70、肝脏病理、血清肝功能生化指标等变化。结果 创伤后血浆皮质醇浓度迅速增加 ,伤后 4h达到峰值 ,2 4h仍维持在高水平 ;肝组织GR的结合容量伤后即开始下降 ,12h降至最低 ,2 4h有所回升 ,HSP70在伤后增加 ,8h达到高峰 ,2 4h仍持续在较高水平 ;但肝脏病理、血清ALT、TB的改变差异无显著性。使用GR阻断剂后 ,血浆皮质醇浓度较严重创伤组明显增加 ,肝淤血明显 ,肝窦内有较多炎性细胞浸润 ;血清ALT、TB在伤后早期即有明显升高 ;肝组织HSP70较单纯创伤组明显增多。结论 GR不足可导致创伤后继发性肝功能不全的发生 ;HSP70参与了肝组织细胞抗损伤机制的启动 ;GC。
Objective To study the effects of glucocorticoid(GC),glucocorticoid receptor(GR),and heat shock protein70(HSP70)on hepatic injury in the early stage of severe trauma.Methods 88 adult male Wistar rats were randomly divided into control group,and severe trauma group,severe trauma with 50% GR blocked group.Rat model was produced by adopting severe thoracic impact injury with unilateral femoral fracture.Dynamic changes of GC in plasma,GR and HSP70 in hepatic tissue,pathology of liver,hepatic function markers in blood serum after severe trauma were observed.Results Cortisol in plasma rapidly increased,reached peak at 4 h after trauma,and maintained rather high level to 24 h.Binding volume of GR gradually decreased in hepatic tissue after severe trauma,reduced to the lowest to 12 h,and gradually recovered at 24 h.HSP70 gradually increased in hepatic tissue after severe trauma,increased to the highest at 8 h,and maintained rather high level at 24 h.But hepatic pathology,ALT,TB in serum didnt change significantly after trauma.After use of GR blocking agent,corrisol in plasma increased,hepatic congestion was obvious,and there were more inflammatory cells infiltrated in hepatic sinusoid.ALT and TB in serum obviously increased in early stage after trauma.There were more HSP70 in liver tissue than simple trauma group.Conclusion GR insufficiency may cause secondary hepatic injury after severe trauma.HSP70 may participate in the initiation of anti-injury mechanism of hepatic tissue cell.It is indicated that GC,GR and HSP70 play an important role ininury and anti-injury mechanism of hepatic tissue cell in secondary hepatic injury after severe trauma.
出处
《中华急诊医学杂志》
CAS
CSCD
2003年第10期664-666,共3页
Chinese Journal of Emergency Medicine
基金
国家重点基础研究发展规划项目 (G19990 5 42 0 0 )
