论文部分内容阅读
肝脏缺血再灌注时,细胞因子、黏附分子等炎症介质趋化聚集中性粒细胞,使它在肝组织中释放大量蛋白水解酶及氧自由基。核因子-κB(NF-κB)能够转录调节再灌注时诱导表达的炎症介质编码基因。NF-κB受到活化时,需要抑制因子核因子一κB抑制蛋白(IκB)的降解,而蛋白酶体抑制剂通过抑制泛素一蛋白酶体途径,减少I κB在蛋白酶体中的降解。本实验采用肝脏部分缺血再灌注模型,研究蛋白酶体抑制剂MG132对NF κB介导的肝缺血再灌注损伤中的保护作用。
Liver ischemia reperfusion, cytokines, adhesion molecules and other inflammatory mediators chemotactic aggregation of neutrophils, it released in the liver tissue a large number of proteolytic enzymes and oxygen free radicals. Nuclear factor-κB (NF-κB) transcriptionally regulates the expression of the inflammatory mediator-encoding genes upon reperfusion. Activation of NF-κB requires inhibition of the degradation of the nuclear factor-κB inhibitor (IκB), a proteasome inhibitor that reduces the degradation of IκB in the proteasome by inhibiting the ubiquitin-proteasomal pathway. In this study, a partial hepatic ischemia-reperfusion model was used to study the protective effect of the proteasome inhibitor MG132 on NF-κB-mediated hepatic ischemia-reperfusion injury.