肝切除诱导c-met受体酪氨酸磷酸化及组织再生的调控机制  

Role of c-met tyrosine phosphorylation on hepatic regeneration and its correlative mechanisms after partial hepatectomy

作　　者：吴向阳[1] 时开网[1] 卞建民[1] 井清源[1] 

机构地区：[1]南京市第一医院普通外科,江苏南京210006

出　　处：《医学研究生学报》2006年第5期431-434,共4页Journal of Medical Postgraduates

摘　　要：目的:探讨部分肝切除(PH)诱导残余肝细胞膜受体c-met酪氨酸磷酸化及肝再生的调控机制。方法: 采用PH建立急性肝损伤再生模型,用免疫沉淀和免疫印迹等方法评价肝损伤后组织再生、功能恢复和c-met酪氨酸磷酸化的变化以及染料木黄酮对它们的影响。结果:急性PH能显著诱导膜受体c-met酪氨酸磷酸化,且在术后1 h升至最高(P<0．05);染料木黄酮能有效减少PH后早期c-met酪氨酸磷酸化,且抑制肝冉生和功能恢复 (P<0．05)。结论:PH可能诱导c-met受体激活,参与肝细胞生长因子(HGF)介导的肝组织再生调控,且残余肝细胞内酪氨酸蛋白激酶的活性上调,对肝组织的再生及其损伤后的功能恢复有明显作用。Objective： To evaluate the acute hepatic failure induced tyrosine phosphorylation of c-met and mechanisms on hepatic regeneration after was induced by partial hepatectomy. Hepatic partial hepatectomy. Methods： The acute hepatic failure regeneration, function recovery, c-met tyrosine phosphorylation and the effect of genistein were observed. Results ： Acute hepatic failure can induced rapid tyrosine phosphorylation of c-met significatively, which can be reduced obviously by administration of genistein （P 〈 0.05 ）. Furthermore, genistein also inhibit hepatic regeneration and function recovery after hepatic lesion through inhibition of tyrosine phosphorylation （ P 〈 0.05 ）. Conclusion ： Partial hepatectomy can induce rapidly tyrosine phosphorylation of c-met, whose activation might involve in regula tion of HGF-induced hepatic regeneration. Tyrosine phosphorylation may play a crucial role in hepatic regeneration and function recovery after acute hepatic failure.

关 键 词：部分肝切除 C-MET 酪氨酸磷酸化 染料木黄酮 

分 类 号：R657.3[医药卫生—外科学]