摘要
目的探讨急性重症胆管炎(ACST)大鼠肝组织高迁移率族蛋白1(HMG-1)改变及其对肿瘤坏死因子(TNF-α)表达的调节作用。方法通过制作ACST大鼠模型,正丁酸钠干预,不同时相点检测肝组织HMG-1及TNF-α表达,同时观察肝功能及结构改变。结果ACST组12～24 h肝组织HMG-1和TNF-αmRNA表达均显著增强(P<0．05或0．01)。正丁酸钠处理可显著抑制ACST后12～24 h肝组织HMG-1 mRNA表达(P<0．01),并明显下调肝组织TNF-αmRNA表达及TNF-α水平(P<0．05或0．01),同时血清谷丙转氨酶(ALT)水平显著降低(P<0．05或0．01),肝脏的病理形态得到明显改善。结论ACST大鼠肝组织HMG-1表达可促进局部TNF-α的合成与释放,从而诱导ACST大鼠急性肝功能损害。
Objective TO observe the changes of high mobility group 1 protein （HMG-1） in the liver of acute cholangitis of severe type（ACST） rats and its modulate role on tumor necrosis factor-α （TNF-α）. Methods ACST rat models were made. Treatment with sodiumbutyrate,and to determine HMG-1/TNF-αmRNA expression in different time, observe the changes of liver function and sturcture in microscopy. Results Both HMG-1 and TNF-αmRNA levels significantly increased in the liver during 12-24 h after ACST（P〈0. 05 or 0. 01）. Treatment with sodiumbutyrate could markedly inhibitrenal HMG-1mRNA expression at 12 h and 24 h following ACST（P〈0. 01 ）, renal TNF-αmRNA as well as protein （P〈0. 05 or 0.01） levels were also decreased. In addition, serum alanine transminase （ALT） in the treatment group was significantly lower than that in ACST group, respectively （P〈 0.05 or 0. 01）. Liver sturcture in microscopy get a significantly prograss. Conclusion Elevation of HMG-1 in the liver might markedly enhance local TNF-αexpression and release, whice would be involved in the development to facute liver function injury as sociated with acute cholangitis of severe type.
出处
《中华肝胆外科杂志》
CAS
CSCD
2006年第12期847-849,共3页
Chinese Journal of Hepatobiliary Surgery
