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 language | English |
|---|---|
| Pages (from-to) | 198-203 |
| Number of pages | 6 |
| Journal | Biochemical and Biophysical Research Communications |
| Volume | 351 |
| Issue number | 1 |
| DOIs | |
| State | Published - 08 12 2006 |
| Externally published | Yes |
Keywords
- Global ischemia
- Hippocampus
- Mitochondria
- Peroxisome proliferator-activated receptor-γ
- Rosiglitazone
- Uncoupling protein 2