Neuroprotective Effects of a Glutathione Depletor in Rat Post-Ischemic Reperfusion Brain Damage

Author(s): Claudia Di Giacomo, Rosa Santangelo, Valeria Sorrenti, Giovanni L. Volti, Rosaria Acquaviva

Journal Name: CNS & Neurological Disorders - Drug Targets
Formerly Current Drug Targets - CNS & Neurological Disorders

Volume 14 , Issue 1 , 2015

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The induction of heme oxygenase (HO), the rate-limiting enzyme in heme degradation, occurs as an adaptative response to oxidative stress and is consequent to decrease in cellular glutathione levels. Our previous studies demonstrated significant increase in survival rates of rats treated with glutathione depletors and submitted to transient cerebral ischemia. The aim of the present research was to test the effects of L-Buthionine sulfoximine (BSO), a glutathione depletor, during cerebral post-ischemic reperfusion. Cerebral ischemia was induced by bilateral clamping of common carotid arteries for 20 min. Each sample was used for glutathione ad lipid peroxidation level dosage and for evaluating the expression of heme oxygenase both after a single subcutaneous administration of BSO and without treatment. In the same experimental conditions, endothelial, inducible and neuronal Nitric Oxide Synthase (eNOS, iNOS and nNOS) and Dimethylarginine Dimethyl amine Hydrolases (DDAH-1 and DDAH-2) were also evaluated. Results obtained in the present study suggested that HO-1 over-expression may be implicated in the protective effect of BSO in post-ischemic reperfusion brain damage, although the involvement of other important stress mediators cannot be ruled out.

Keywords: L-Buthionine sulfoximine, cerebral ischemia, glutathione, heme oxygenase, nitric oxide, reperfusion.

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Article Details

Year: 2015
Published on: 01 February, 2015
Page: [41 - 48]
Pages: 8
DOI: 10.2174/1871527314666150116113647

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