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

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 ra...

Full description

Saved in:
Bibliographic Details
Published in:Biochemical and biophysical research communications 2006-12, Vol.351 (1), p.198-203
Main Authors: Chen, Shang-Der, Wu, Hsin-Yi, Yang, Ding-I, Lee, Su-Ying, Shaw, Fu-Zen, Lin, Tsu-Kung, Liou, Chia-Wei, Chuang, Yao-Chung
Format: Article
Language:English
Subjects:
60 APPLIED LIFE SCIENCES
Animals
Global ischemia
HIPPOCAMPUS
Hippocampus - blood supply
Hippocampus - drug effects
Hippocampus - metabolism
Hippocampus - pathology
INFLAMMATION
INJURIES
Ion Channels - metabolism
ISCHEMIA
Ischemic Attack, Transient - metabolism
Ischemic Attack, Transient - pathology
LIGANDS
LIPIDS
Male
MITOCHONDRIA
Mitochondrial Proteins - metabolism
Peroxisome proliferator-activated receptor-γ
PPAR gamma - antagonists & inhibitors
RATS
Rats, Sprague-Dawley
RECEPTORS
Rosiglitazone
Thiazolidinediones - pharmacology
Uncoupling Protein 2
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary: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.
ISSN:0006-291X
1090-2104
DOI:10.1016/j.bbrc.2006.10.017