Dragin Nadine, Smani Moneïm, Arnaud-Dabernat Sandrine, Dubost Clément, Moranvillier Isabelle, Costet Pierre, Daniel Jean-Yves, Peuchant Evelyne
EA 3674 - Laboratoire de Biologie de la Différenciation et du Développement, Université de Bordeaux 2, 146 Rue Léo-Saignat, 33076 Bordeaux Cedex, France.
FEBS Lett. 2006 Jul 10;580(16):3845-52. doi: 10.1016/j.febslet.2006.06.006. Epub 2006 Jun 15.
Oxidative stress is known to produce tissue injury and to activate various signaling pathways. To investigate the molecular events linked to acute oxidative stress in mouse liver, we injected a toxic dose of paraquat. Liver necrosis was first observed, followed by histological marks of cell proliferation. Concomitantly, activation of the MAP kinase pathway and increased levels of the anti-apoptotic protein Bcl-XL were observed. Gene expression profiles revealed that the differentially expressed genes were potentially involved in cell proliferation. These data suggest that paraquat-induced acute oxidative stress triggers the activation of regeneration-related events in the liver.
已知氧化应激会导致组织损伤并激活各种信号通路。为了研究与小鼠肝脏急性氧化应激相关的分子事件，我们注射了致死剂量的百草枯。首先观察到肝脏坏死，随后出现细胞增殖的组织学特征。同时，观察到丝裂原活化蛋白激酶（MAP）激酶途径的激活以及抗凋亡蛋白Bcl-XL水平的升高。基因表达谱显示，差异表达的基因可能参与细胞增殖。这些数据表明，百草枯诱导的急性氧化应激触发了肝脏中与再生相关事件的激活。
