Naslov
Pioglitazone limits the cortical oxidative damage following traumatic brain injury in the rat

Autori
Pilipović, Kristina ; Frković, Vedran ; Dangubić, Boban ; Župan, Željko ; Peternel, Sandra ; Župan, Gordana

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

Izvornik
Periodicum Biologorum, Vol. 109, Suppl. 2, Abstracts of the 5th Croatian Congress of Pharmacology and 2nd Congress of Croatian Physiological Society / Banfić, H. ; Boban, M. ; Francetić, I. ; Klarica, M. ; Mück-Šeler, D. ; Pivac, N. ; Sabolić, I. ; Tvrdeić, A. ; Župan, G. - Zagreb : Hrvatsko prirodoslovno društvo, 2007, 122-122

Skup
5th Croatian Congress of Pharmacology and 2nd Congress of Croatian Physiological Society

Mjesto i datum
Osijek, Hrvatska, 19.09.2007. - 22.09.2007

Vrsta sudjelovanja
Poster

Vrsta recenzije
Domaća recenzija

Ključne riječi
Pioglitazone; Traumatic brain injury; Rat

Sažetak
The tissue and cell damage induced by traumatic brain injury (TBI) results from primary damage and from a complex secondary cascade of events including oxidative stress, inflammation, increased vascular permeability, mitochondrial dysfunction and excitotoxic damage. There is no standard pharmacological treatment that blocks the progression of this secondary injury and the current management of TBI is mainly supportive. The peroxisome proliferator-activated receptor-γ (PPAR-γ ) is a member of nuclear receptor superfamily involved in different cellular processes such as regulation of oxidative stress and inflammatory response. Agonists of PPAR-γ have already shown the beneficial effects in the stroke and the spinal cord injury models. This work was performed in order to determine the effects of pioglitazone, a PPAR-γ agonist, on the level of antioxidant enzyme activities and the lipid oxidative damage in the parietal cortex 24 hrs after the induction of TBI in the rat. Experiments were performed on adult male Wistar rats. TBI of moderate severity was induced using the lateral fluid percussion (LFP) brain injury model. Briefly, rats were placed in a stereotactic frame and surgically prepared for LFP brain injury or sham operation as previously described (Mcintosh et ai, 1989). A 5-mm craniotomy was performed over the left parietal cortex, between lambda and bregma sutures, leaving the dura mater intact. A hollow female Luer Lock fitting was positioned over the craniotomy and held in place with dental cement. Animals were attached to the LFP device and brain injury was induced by a rapid injection of a pressure pulse of saline. Animals were i.p. injected with either pioglitazone (1 mg/kg) or vehicle 10 min after the TBI. Sham-operated, vehicle-treated animals were used as the control group. Rats were sacrificed 24 hrs after the TBI induction. Activities of antioxidant enzymes superoxide dismutase (SOD) and glutathione peroxidase (GPX) were determined by standard spectrophotometric measurements. Levels of the brain lipid peroxidation were determined by thiobarbituric acid reactive substances (TBARS) assay. TBI caused the significant increases of the GPX activity and the TBARS level, and a slight decrease of the SOD activity in the injured parietal cortex. Pioglitazone treatment resulted in the additional increase of GPX activity and in the decrease of the TBARS level in the examined cortical region of injured rats. Our findings demonstrate the activation of the antioxidant enzymatic system and the intense oxidative damage of lipids in ipsilateral parietal cortex following TBI. These results also suggest a protective role of pioglitazone in the brain oxidative damage in our experimental conditions.

Izvorni jezik
Engleski

Znanstvena područja
Temeljne medicinske znanosti

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