休克期切痂对烫伤大鼠肝HMGB1表达及肝功能的影响

目的　探讨休克期切痂对烫伤大鼠肝组织高迁移率族蛋白B1(HMGBl)表达及肝脏功能影响。方法　 30 %Ⅲ度烫伤Wistar大鼠随机分为 2 4h和 72h切痂植皮组。RT PCR和免疫组化染色法检测肝脏HMGBlmRNA/蛋白表达 ,同时检测血浆AST、ALT含量。结果　大鼠烫伤后肝组织HMGB1mRNA表达量增加 1～ 2 5倍 ,2 4h切痂组伤后 8d其水平较烫伤对照和 72h切痂组显著减少 (P <0 0 5 )。烫伤后大鼠肝细胞和枯否细胞HMGB1表达阳性率较正常大鼠均显著升高 (P <0 0 1) ,2 4h切痂组 4、 8dHMGB1表达阳性细胞数较烫伤对照和 72h切痂组均显著减少 (P <0 0 1)。同时 ,烫伤大鼠血浆AST和ALT水平升高 (P<0 0 5 ) ,而 2 4h切痂组伤后 4、 8d较烫伤对照组和 72h切痂组显著降低 (P <0 0 1)。结论　烫伤大鼠休克期切痂能够下调肝组织HMGB1表达 ,局部HMGB1诱生参与了肝损伤的病理生理过程。

Effects of escharectomy during shock stage on high mobility group box-1 chromosomal protein (HMGB1)expression and hepatic function in burned rats

Objective To investigate the effects of escharectomy during shock stage on the expression of hepatic HMGB 1 in rats following thermal injury. Methods Wistar rats inflicted by 30% full-thickness burned injury were randomly distributed to 24 h escharectomy group and 72 h escharectomy group, in which escharectomy was performed at 24 and 72 hours post-burn, respectively.Expression of HMGB1 in liver was assured with RT-PCR and immunohistochemistry, and plasma AST and ALT levels were also measured.Results Hepatic HMGB1 mRNA expression increased by 1- to 2.5-fold after thermal injury in rats.It was markedly reduced in animals of 24 h escharectomy group compared with those of burn controls as well as 72 h escharectomy group on post-burn day 8 (z=2.423,P= 0.015 or z=2.063,P=0.039, respectively). HMGB1 protein expression in hepatocytes and Kupffer's cells of burned rats was significantly up-regulated compared with that of normal controls (P<0.05), Plasma AST and ALT levels were significantly higher in burned animals than that in normal controls (P<0.05). The positive rate of HMGB1 expression in hepatocytes and Kupffer's cells, as well as the levels of plasma AST and ALT were higher in animals of 24 h escharectomy group than those in normal animals, but they were reduced significantly compared with controls and 72 h escharectomy group on post-burn day 4 and 8 (P<0.05 or P<0.01). Conclusion Escharectomy during shock stage could down-regulate hepatic HMGB1 expression together with improvement of liver function in burned rats. Excessive HMGB1 formation in liver might be involved in the pathogenesis of acute hepatic injury secondary to major burns.