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Acta Physiologica 2008; Volume 194, Supplement 665
The 59th National Congress of the Italian Physiological Society
9/17/2008-9/19/2008
Cagliari, Italy
NEUROPROTECTIVE ACTION OF RESVERATROL AGAINST OXIDATIVE STRESS IN THE MPTP MOUSE MODEL OF PARKINSON'S DISEASE
Abstract number: OC20
BONOMO1 A, KAIRISALO2 M, KORHONEN2 L, LINDHOLM2 D, BELLUARDO1 N, MUDO1 G
1Dept. of Experimental Medicine, div. of Human Physiology, University of Palermo, corso Tukory 129, Palermo, Italy
2Minerva Institute for Medical Research, Biomedicum Helsinki, Helsinki, [email protected]
Aim:
To study the potential in vivo neuroprotective properties of the natural antioxidant product resveratrol we have investigated the ability of this compound to protect dopaminergic neurons against the cellular insult of oxidative stress in the MPTP model.
Methods:
C57BL/6 mice received four intraperitoneal (i.p.) injections of MPTP (14 mg/kg) at 90 min intervals. Resveratrol was given at dose of 20 mg/kg i.p. with the following treatment scheme: 30 min before MPTP treatment and 12 h following the last dose of MPTP and every 24 h for three days.
Results:
The number of TH-positive neurons in the substantia nigra (SN) and the expression level of TH in the striatum of MPTP treated mice were significantly reduced by 65% and 70% respectively at 7 days after injection of MPTP. In MPTP mice treated with resveratrol the number of TH-positive neurons in the SN and TH expression level in the striatum were decreased only by 35% and 30% respectively. The DAT expression levels in the striatum confirmed the neuroprotective effect of resveratrol in MPTP treated mice and revealed a significant up-regulation of DAT levels in control mice treated with resveratrol. Studying the mechanism we observed that resveratrol protected PC6.3 neuronal cells against oxidative stress and increased the levels of the anti-apoptotic protein XIAP in the cells.
Conclusions:
Our data show that resveratrol can protect SN against MPTP cytotoxicity and this may be of biological importance in considering novel therapies for Parkinson's disease.
To cite this abstract, please use the following information:
Acta Physiologica 2008; Volume 194, Supplement 665 :OC20