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

Journal Article · Fri Dec 08 00:00:00 EST 2006 · Biochemical and Biophysical Research Communications

DOI:https://doi.org/10.1016/j.bbrc.2006.10.017· OSTI ID:20857905

Chen, S -D ^[1]; Wu, H -Y ^[2]; Yang, D -I ^[3]; Lee, S -Y ^[1]; Shaw, F -Z ^[4]; Lin, T -K ^[1]; Liou, C -W ^[1]; Chuang, Y -C ^[1]

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1. Department of Neurology, Chang Gung Memorial Hospital-Kaohsiung Medical Center, Chang Gung University College of Medicine, Taiwan (China)
2. Center for Neuroscience, National Sun Yat-sen University, Kaohsiung, Taiwan (China)
3. Institute of Brain Science, National Yang-Ming University, Taipei, Taiwan (China)
4. Institute of Cognitive Science, National Cheng Kung University, Tainan, Taiwan (China)

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} {sup {yields}} UCP2 {sup {yields}} neuroprotection' cascade in ischemic brain injury.

• OSTI ID: 20857905
• Journal Information: Biochemical and Biophysical Research Communications, Vol. 351, Issue 1; Other Information: DOI: 10.1016/j.bbrc.2006.10.017; PII: S0006-291X(06)02253-4; Copyright (c) 2006 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
• Country of Publication: United States
• Language: English

Related Subjects

60 APPLIED LIFE SCIENCES
HIPPOCAMPUS
INFLAMMATION
INJURIES
ISCHEMIA
LIGANDS
LIPIDS
MITOCHONDRIA
RATS
RECEPTORS