中文摘要：

在创伤 / 出血性的吃惊(T/HS ) 在肺损害和 apoptosis 上决定白朊管理的效果的目的老鼠。工作方法研究被执行在上一在里面自发地与导致的 T/HS 呼吸老鼠的 vivo 模型；老鼠与 Ringer 的家为 20 min 受到腿节骨折，为 30 min 的局部缺血，和灌注喂奶答案(RS ) 或 5%(w/v ) 白朊(白长袍的) ，和肺的左更低的脑叶是 resected。显著地在灌注期间管理的结果白朊稀释了肺的损害并且减少乳的酸的集中和数字在 situ 标记的调停 TdT 的 dUTP 刻痕结束(TUNEL ) 积极房间。而且，在灌注在原子因素的水平揭示了增加以后，免疫组织化学执行了 24 h κB (NF-κB ) ，和在白朊未经治疗的组的激活 mitogen 的蛋白质 kinase (MAPK ) 是的 phosphorylated p38 由白朊处理下面调整什么时候与假冒的老鼠相比。有白朊的结论复活稀释织物损害并且经由工作刺激 NF-κB 的激活的 p38 MAPK 信号 transduction 小径在肺禁止 T/HS-induced apoptosis。

英文摘要：

Objective： To determine the effects of albumin administration on lung injury and apoptosis in traumatic/hemorrhagic shock （T/HS） rats. Methods： Studies were performed on an in vivo model of spontaneously breathing rats with induced T/HS; the rats were subjected to femur fracture, ischemia for 30 min, and reperfusion for 20 min with Ringer＇s lactate solution （RS） or 5% （w/v） albumin （ALB）, and the left lower lobes of the lungs were resected. Results： Albumin administered during reperfusion markedly attenuated injury of the lung and decreased the concentration of lactic acid and the number of in situ TdT-mediated dUTP nick-end labelling （TUNEL）-positive cells. Moreover, immunohistochemistry performed 24 h after reperfusion revealed increases in the level of nuclear factor κB （NF-κB）, and phosphorylated p38 mitogen-activated protein kinase （MAPK） in the albumin-untreated group was down-regulated by albumin treatment when compared with the sham rats. Conclusion： Resuscitation with albumin attenuates tissue injury and inhibits T/HS-induced apoptosis in the lung via the p38 MAPK signal transduction pathway that functions to stimulate the activation of NF-κB.