期刊文献+

动态监测STAT3、HMGB1在急性肝衰竭大鼠中的变化及意义 被引量:1

Dynamic changes of STAT3 and HMGB1 in acute liver failure rats
原文传递
导出
摘要 目的观察信号转导子和转录激活因子(STAT3),高迁移率族蛋白B1(HMGB1)在D-氨基半乳糖介导急性肝衰竭模型中的动态变化规律。方法用D-氨基半乳糖制作大鼠急性肝衰竭模型,用RT-PCR检测STAT3mRNA,HMGB1mRNA在急性肝衰竭大鼠肝组织6、12、24、48、72、120和168h的表达。结果STAT3 mRNA在急性肝衰竭的6h有显著升高,与正常组差异有统计学意义(P<0.01),24h达高峰,在48、72、120h仍保持较高水平,与正常组比较差异有统计学意义(P<0.01);HMGB1 mRNA在6h亦显著升高,与正常组比较差异有统计学意义(P<0.01),12h达高峰,在24、48、72h仍保持较高水平,与正常组比较差异有统计学意义(P<0.01)。ALT和AST在6h有轻度升高,至24h与正常组差异有统计学意义(P<0.05),48h(P<0.01)达高峰,72h逐渐下降。TBil在6h开始持续升高,72h达到高峰(P<0.01),120h逐渐下降。结论STAT3、HMGB1可能参与了急性肝衰竭的病理生理过程,可能成为临床上治疗急性肝衰竭的新靶点。 Objective To observe the develolxnent of STAT3 and HMGB1 in acute liver failure rats induced by D-galactosamine. Method Acute liver failure rats were induced by injecting of D-galactosamine, the expressions of SrAT3 mRNA and HMGB1 mRNA were detected by reverse transcription polymerase chain reation at 6, 12, 24, 48, 72,120, 168 hours. Results The expression of STAT3 mRNA increased obviously at 6 hours ( P 〈 0.01) and reached to the peak at 24 hours. There were statistical differences with the normal group at 48, 72 and 120 hours( P 〈 0.01 ). The expression of HMGB1 mRNA also increased obviously at 6 hours ( P 〈 0.01 ) and reached to the peak at 12 hours. There were statistical differences with the normal group at 24, 48 and 72 hours( P 〈 0.01). ALT and AST increased slightly at 6 hours and there was statistical significance with the normal group at 24 hours( P 〈 0.05), reached to the peak at 48 - hours( P 〈 0.01 ), began to decrease at 72 hours point. Total bilirubin began to increase at 6, reached to the peak at 72 hours(P 〈0.01), began to decrease at 120 hours. Conclusions ST AT3 and HMGB1 are intimately associated with actue liver failure. They may become a new target in clinical treatment.
出处 《国际流行病学传染病学杂志》 CAS 2009年第1期8-11,共4页 International Journal of Epidemiology and Infectious Disease
基金 温州市科技计划项目(Y20080155)
关键词 肝功能衰竭 急性 D-氨基半乳糖 监测 Liver failure, acute D-galactosamine Surveillance
  • 相关文献

参考文献7

二级参考文献14

共引文献31

同被引文献7

引证文献1

二级引证文献5

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部