CAJ | 학술논문

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STAT3 mRNA,HNCB1 mRNA在急性肝衰竭大鼠肝组织6、12、24、48、72、120和168 h的表达.结果 STAT3 mRNA在急性肝衰竭的6 h有显著升高,与正常组差异有统计学意义(P<0.01),24 h达高峰,在48、72、120 h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6 h亦显著升高,与正常组比较差异有统计学意义(P<0.01),12 h达高峰,在24、48、72 h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6 h有轻度升高,至24 h与正常组差异有统计学意义(P<0.05),48 h(P<0.01)达高峰,72 h逐渐下降.TBil在6 h开始持续升高,72 h达到高峰(P<0.01),120 h逐渐下降.结论 STAT3、HNGB1可能参与了急性肝衰竭的病理生理过程,可能成为l临床上治疗急性肝衰竭的新靶点.
목적 관찰신호전도자화전록격활인자(STAT3),고천이솔족단백B1(HMGB1)재D-안기반유당개도급성간쇠갈모형중적동태변화규률.방법 용D-안기반유당제작대서급성간쇠갈모형,용RT-PCR검측STAT3 mRNA,HNCB1 mRNA재급성간쇠갈대서간조직6、12、24、48、72、120화168 h적표체.결과 STAT3 mRNA재급성간쇠갈적6 h유현저승고,여정상조차이유통계학의의(P<0.01),24 h체고봉,재48、72、120 h잉보지교고수평,여정상조비교차이유통계학의의(P<0.01);HMGB1 mRNA재6 h역현저승고,여정상조비교차이유통계학의의(P<0.01),12 h체고봉,재24、48、72 h잉보지교고수평,여정상조비교차이유통계학의의(P<0.01).ALT화AST재6 h유경도승고,지24 h여정상조차이유통계학의의(P<0.05),48 h(P<0.01)체고봉,72 h축점하강.TBil재6 h개시지속승고,72 h체도고봉(P<0.01),120 h축점하강.결론 STAT3、HNGB1가능삼여료급성간쇠갈적병리생리과정,가능성위l림상상치료급성간쇠갈적신파점.
Objective To observe the development of STAT3 and HMGB1 in acute liver failure tats induced by D-galactosamine. Method Acute liver failure rats were induced by injecting of D-galactosamine, the expressions of STAT3 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 at48, 72 and 120 hours(P<0.01). 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.Conclusion STAT3 and HMGB1 are intimately associated with actue liver failure. They may become a new target in clinical treatment.