Autophagy is upregulated in rats with status epilepticus and partly inhibited by Vitamin E

被引:56
作者
Cao, Lili [1 ]
Xu, Jingjing [1 ]
Lin, Youting [1 ]
Zhao, Xiuhe [1 ]
Liu, Xuewu [1 ]
Chi, Zhaofu [1 ]
机构
[1] Shandong Univ, Qilu Hosp, Dept Neurol, Jinan 250012, Peoples R China
关键词
Autophagy; Light chain 3; Beclin; 1; Oxidative stress; Hippocampus; CELL-DEATH; OXIDATIVE STRESS; WISTAR RATS; PILOCARPINE; SYSTEM; HIPPOCAMPUS; BECLIN-1; TUMORIGENESIS; ACTIVATION; PATHWAY;
D O I
10.1016/j.bbrc.2008.12.178
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Autophagy, a process of bulk degradation of cellular constituents through autophagosome-lysosomal pathway, is enhanced during oxidative stress. Whether autophagy is induced during Status epilepticus (SE), which induces an excess production of reactive oxygen species (ROS) and leads to oxidative stress, is not established. We also Sought to determine if pretreatment with Vitamin E reduced autophagy. We used pilocarpine to elicit SE in rats. The ratio of LC3 II to LC3 I and beclin 1 were used to estimate autophagy. We found that ratio of LC3 11 to LC3 I and beclin I increased significantly at 2, 8, 16, 24 and 72 h, peaking at 24 h after SE onset. Pretreatment with Vitamin E partially inhibited autophagy by reducing LC3 II formation and de novo synthesis of beclin 1 at 24 h after seizures. These data show that autophagy is increased in rats with pilocarpine-induced SE, and Vitamin E have a partial inhibition on autophagy. (C) 2009 Elsevier Inc. All rights reserved.
引用
收藏
页码:949 / 953
页数:5
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