Naslov
Effects of PPAR-γ agonist pioglitazone on the hippocampus in traumatic brain injured rats

Autori
Župan, Gordana ; Pilipović, Kristina ; Župan, Željko ; Frković, Vedran ; Dangubić, Boban ; Mršić-Pelčić, Jasenka ; Šustić, Alan

Vrsta, podvrsta i kategorija rada
Sažeci sa skupova, sažetak, znanstveni

Izvornik
Abstracts of the 13th Congress of the European Federation of Neurological Societies ; u: European Journal of Neurology. Volume 16 (2009) (S3) / Hillbom, Matti ; Schapira, Anthony - Firenza : München : Wiley-Blackwell, 2009, 605-605

Skup
13th Congress of the European Federation of Neurological Societies

Mjesto i datum
Firenca, Italija, 12.09.2009. - 15.09.2009

Vrsta sudjelovanja
Poster

Vrsta recenzije
Međunarodna recenzija

Ključne riječi
traumatic brain injury; enoxaparin; oxidative stress; antioxidant enzymes; COX-2; rats

Sažetak
Background and aim: Agonist of the peroxisome proliferator-activated receptor-gama (PPAR-γ), pioglitazone, exerts protective role in several experimental models of CNS diseases, such as focal cerebral ischemia, Parkinson's disease, allergic encephalitis, Alzheimer's disease, temporal lobe epilepsy. Its effects in traumatic brain injury (TBI) models are not known. In this study we determined the levels of lipid oxidative damage, the activities of antioxidant enzymes and inflammation parameter expression in the hippocampi of rats with TBI, and treated by a single dose of pioglitazone. Methods: Experiments were performed on adult male Wistar rats. TBI of moderate severity was performed over the left parietal cortex using the lateral fluid percussion brain injury model. Animals were i.p. injected with either pioglitazone (1 ; 3 mg/kg) or vehicle 10 min after TBI. Sham-operated, vehicle-treated animals were used as the control group. Rats were sacrificed 24 hrs after the TBI induction and the hippocampi were processed for spectrophotometric measurements of the thiobarbituric acid reactive substances (TBARS) levels, the superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities or for the analyses of COX-2 expressions. Results: TBI caused the significant increases of the TBARS level, the GSH-Px activity, and COX-2 expression while pioglitazone treatment induced the decrease in lipid oxidative damage and the increases of both antioxidant enzymes’ activities in the ipsilateral hippocampus. TBI-induced COX-2 overexpression was not influenced by pioglitazone administration in mentioned brain structure. Conclusion: Our preliminary results for the first time suggest neuroprotective effects of a single dose of pioglitazone on TBI-induced oxidative hippocampal damage.

Izvorni jezik
Engleski

Znanstvena područja
Temeljne medicinske znanosti

POVEZANOST RADA