Mitochondria-targeted plastoquinone antioxidant SkQR1 decreases trauma-induced neurological deficit in rat

• Published in: Biochemistry (Moscow) Vol. 77; no. 9; pp. 996 - 999
• Main Authors: Isaev, N. K., Novikova, S. V., Stelmashook, E. V., Barskov, I. V., Silachev, D. N., Khaspekov, L. G., Skulachev, V. P., Zorov, D. B.
• Format: Journal Article
• Language: English
• Published: Dordrecht SP MAIK Nauka/Interperiodica 01.09.2012; Springer; Springer Nature B.V
• Subjects: Animals; Antioxidants; Antioxidants - metabolism; Antioxidants - pharmacology; Biochemistry; Biomedical and Life Sciences; Biomedicine; Bioorganic Chemistry; Brain; Brain Injuries - drug therapy; Brain Injuries - pathology; Electron transport; Life Sciences; Magnetic Resonance Imaging; Male; Microbiology; Mitochondria; Mitochondria - metabolism; Mitochondrial DNA; Neurology; Neuroprotective Agents - metabolism; Neuroprotective Agents - pharmacology; Plastoquinone - analogs & derivatives; Plastoquinone - metabolism; Plastoquinone - pharmacology; Rats; Rats, Wistar; Rhodamines - metabolism; Rhodamines - pharmacology; mitochondria-targeted antioxidants; SkQR1; brain trauma; neuroprotection
• ISSN: 0006-2979; 1608-3040
• DOI: 10.1134/S0006297912090052

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.