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Mitochondria-Targeted Plastoquinone Antioxidant SkQR1 Decreases Trauma-Induced Neurological Deficit in Rat

N. K. Isaev1,2,3*, S. V. Novikova2,3, E. V. Stelmashook2,3, I. V. Barskov2, D. N. Silachev1,3, L. G. Khaspekov2, V. P. Skulachev1,3, and D. B. Zorov1,3

1Belozersky Institute of Physico-Chemical Biology, Lomonosov Moscow State University, 119991 Moscow, Russia; fax: (495) 939-3181; E-mail: isaev@genebee.msu.ru

2Research Center of Neurology, Russian Academy of Medical Sciences, Volokolamskoe Shosse 80, 125367 Moscow, Russia

3Institute of Mitoengineering, Lomonosov Moscow State University, 119991 Moscow, Russia

* To whom correspondence should be addressed.

Received March 14, 2012; Revision received June 18, 2012
A protective effect of a mitochondria-targeted antioxidant, a cationic rhodamine derivative linked to a plastoquinone molecule (10-(6′-plastoquinonyl)decylrhodamine-19, SkQR1) was studied in the model of open focal trauma of rat brain sensorimotor cortex. It was found that daily intraperitoneal injections of SkQR1 (100 nmol/kg) for 4 days after the trauma improved performance in a test characterizing neurological deficit and decreased the volume of the damaged cortical area. Our results suggest that SkQR1 exhibits profound neuroprotective effect, which may be explained by its antioxidative activity.
KEY WORDS: brain trauma, neuroprotection, mitochondria-targeted antioxidants, SkQR1

DOI: 10.1134/S0006297912090052