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

Shang Der Chen, Hsin Yi Wu, Ding I. Yang, Su Ying Lee, Fu Zen Shaw, Tsu Kung Lin, Chia Wei Liou, Yao Chung Chuang

Research output: Contribution to journalArticlepeer-review

40 Citations (Scopus)

Abstract

We investigate the effect of rosiglitazone, a ligand for peroxisome proliferator-activated receptor-γ (PPARγ) 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 "PPARγ → UCP2 → neuroprotection" cascade in ischemic brain injury.

Original languageEnglish
Pages (from-to)198-203
Number of pages6
JournalBiochemical and Biophysical Research Communications
Volume351
Issue number1
DOIs
Publication statusPublished - 2006 Dec 8

All Science Journal Classification (ASJC) codes

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology
  • Psychology(all)

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