Hierholzer C, Kalff J C, Bednarski B, Memarzadeh F, Kim Y M, Billiar T R, Tweardy D J
Department of Surgery, University of Pittsburgh School of Medicine and the University of Pittsburgh Cancer Institute, University of Pittsburgh Medical Center, Pittsburgh, PA 15213, USA.
Arch Orthop Trauma Surg. 1999;119(5-6):332-6. doi: 10.1007/s004020050421.
The inflammatory response of the liver to hemorrhagic shock includes the production of acute phase proteins and a variety of mediators, such as the cytokine interleukin (IL)-6. The transcription of acute phase protein genes in hepatocytes has been shown to be activated by Stat3, one of six distinct signal transducers and activators of transcription (STAT) proteins. IL-6 signals through activation of Stat3. In this study, we examined whether or not Stat3 was activated and IL-6 mRNA produced in the liver of rats subjected to hemorrhagic shock and whether or not both phases of shock, the ischemic and the resuscitation phases, were required. We report here that Stat3 activation and increased IL-6 expression required resuscitation and displayed identical kinetics following resuscitation, suggesting that liver production of IL-6 was responsible for liver Stat3 activation in hemorrhagic shock.
肝脏对失血性休克的炎症反应包括急性期蛋白和多种介质的产生，如细胞因子白细胞介素（IL）-6。肝细胞中急性期蛋白基因的转录已被证明可由信号转导子和转录激活子（STAT）六种不同蛋白之一的Stat3激活。IL-6通过激活Stat3发出信号。在本研究中，我们检查了失血性休克大鼠肝脏中Stat3是否被激活以及是否产生了IL-6 mRNA，以及休克的两个阶段，即缺血期和复苏期是否都是必需的。我们在此报告，Stat3激活和IL-6表达增加需要复苏，并且在复苏后呈现相同的动力学，这表明在失血性休克中肝脏产生的IL-6是肝脏Stat3激活的原因。
