Antioxidant and antiapoptotic actions of selegiline protect against 3-NP-induced neurotoxicity in rats

Antioxidant and antiapoptotic actions of selegiline protect against 3-NP-induced neurotoxicity in... The present study was designed to investigate the neuroprotective effect of selegiline on 3-nitropropionic acid (3-NP)-induced neurotoxicity. Selegiline was intraperitoneally injected at doses 2.5, 5, and 10 mg/kg, 3 days prior to and continued daily, 30 min before 3-NP administration. 3-NP (20 mg/kg, i.p.) was administered for four consecutive days. 3-NP-treated rats exhibited PPI deficits, locomotor hypoactivity, increased striatal and cortical lipid peroxidation, and reduced respective glutathione (GSH) levels as well as catalase and superoxide dismutase (SOD) activities. Changes in the level of the apoptotic regulatory gene expressions were demonstrated as increased striatal and cortical caspase-3 and Bax and decreased respective Bcl2. The two higher dose levels of selegiline (5 and 10 mg/kg) significantly increased locomotor activity, improved prepulse inhibition (PPI), reduced striatal and cortical lipid peroxidation, caspase-3, and Bax, and increased GSH level, catalase, and superoxide dismutase activities and Bcl2 expression. Selegiline at dose 2.5 mg/kg could only reverse some of the manifestations of 3-NP-induced neurotoxicity. Histological examination further affirmed the neuroprotective effect of the higher dose levels of selegiline against 3-NP-induced toxicity. Taken together, these results suggest that selegiline could attenuate 3-NP-induced neurotoxicity. This can be attributed to, at least partly, its antioxidant and antiapoptotic effects. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Naunyn-Schmiedeberg's Archives of Pharmacology Springer Journals

Antioxidant and antiapoptotic actions of selegiline protect against 3-NP-induced neurotoxicity in rats

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Publisher
Springer Berlin Heidelberg
Copyright
Copyright © 2017 by Springer-Verlag GmbH Germany
Subject
Biomedicine; Pharmacology/Toxicology; Neurosciences
ISSN
0028-1298
eISSN
1432-1912
D.O.I.
10.1007/s00210-017-1392-1
Publisher site
See Article on Publisher Site

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