Effects of rosiglitazone on global ischemia-induced hippocampal injury and expression of mitochondrial uncoupling protein 2

被引：50
作者：
Chen, Shang-Der
Wu, Hsin-Yi
Yang, Ding-I
Lee, Su-Ying
Shaw, Fu-Zen
Lin, Tsu-Kung
Liou, Chia-Wei
Chuang, Yao-Chung
机构：
[1] Natl Sun Yat Sen Univ, Ctr Neurosci, Kaohsiung 80424, Taiwan
[2] Natl Yang Ming Univ, Inst Brain Sci, Taipei 112, Taiwan
[3] Natl Cheng Kung Univ, Inst Cognit Sci, Tainan 70101, Taiwan
来源：
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2006年 / 351卷 / 01期
关键词：
global ischemia; hippocampus; mitochondria; peroxisome proliferator-activated receptor-gamma; rosiglitazone; uncoupling protein 2;
D O I：
10.1016/j.bbrc.2006.10.017
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：
We investigate the effect of rosiglitazone, a ligand for peroxisome proliferator-activated receptor-gamma (PPAR gamma) with anti-inflammatory and anti-oxidative actions, on hippocampal injury and its roles in mitochondrial uncoupling protein 2 (UCP2) expression caused by transient global ischemia (TGI) in rats. Increased UCP2 expression was observed in mitochondria of hippocampal CA1 2-24 h after TGI/reperfusion, with maximal expression levels at 6-18 h. Administration of rosiglitazone to hippocampus 30 min prior to the onset of TGI further enhanced mitochondrial UCP2 expression 2-6 h following TGI/reperfusion. Rats subjected to TGI/reperfusion displayed a significant increase in lipid peroxidation, based on increased malondialdehyde (MDA) levels, in hippocampal CA1 mitochondria 2-6 h after reperfusion. Rosiglitazone significantly attenuated TGI/reperfusion -induced lipid peroxidation and suppressed hippocampal CA1 neuronal death based on the surviving neuronal counts. In conclusion, our results provide correlative evidence for the "PPAR gamma -> UCP2 -> neuroprotection" cascade in ischemic brain injury. (c) 2006 Elsevier Inc. All rights reserved.
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收藏
页码：198 / 203
页数：6
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