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目的 探讨严重创伤后早期热休克蛋白 70 (heatshockprotein ,HSP70 )在肝组织中的表达变化 ,及其在肝脏继发性损伤中的作用。方法 成年雄性Wistar大鼠 176只 ,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 2 4h大鼠肝组织HSP70、肝脏病理、血清肝功能生化指标等变化。结果 HSP70在肝组织中表达伤后迅速增加 ,8h达到峰值 ,2 4h仍维持在较高水平。但肝脏病理、血清ALT及TB的改变无显著差异。使用Ru4 86阻断糖皮质激素受体再致伤后 ,肝组织HSP70表达较单纯创伤组明显增多 ;肝窦内有较多炎性细胞浸润 ;血清ALT及TB在伤后早期即有明显升高。结论 HSP70可能参与了肝组织细胞抗损伤机制的启动 ,但HSP70过高表达 ,则可能对肝脏造成损害。HSP70可较好反映创伤后肝损伤与抗损伤这一病理生理过程
Objective To investigate the expression changes of heat shock protein 70 (HSP70) in the liver tissue after severe traumatic injury and its role in secondary liver injury. Methods One hundred and sixty-six adult male Wistar rats were subjected to severe thoracic injury with unilateral femoral fracture. Dynamic changes of HSP70, liver pathology and biochemical indexes of serum liver function were observed dynamically at 24 hours after trauma. Results The expression of HSP70 in the liver tissue increased rapidly after injury, reaching the peak at 8h and remained at a high level at 24 h. However, liver pathology, serum ALT and TB changes no significant difference. Ru4 86 block glucocorticoid receptor re-injury, liver tissue HSP70 expression was significantly increased compared with simple trauma group; sinusoidal sinusitis more inflammatory cell infiltration; serum ALT and TB in the early post-injury significantly increased . Conclusion HSP70 may be involved in the initiation of anti-injury mechanism of liver cells, but over-expression of HSP70 may cause liver damage. HSP70 can better reflect the post-traumatic liver injury and anti-injury pathophysiological process