Neuroprotective effects of spermine following hypoxic-ischemic-induced brain damage: A mechanistic study ANDREW N. CLARKSON, HANZHONG LIU, LACHLAN PEARSON, MOHIT KAPOOR, JOANNA C. HARRISON, IVAN A. SAMMUT, DAVID M. JACKSON and IAN APPLETON 1 Department of Pharmacology and Toxicology, University of Otago, Dunedin, New Zealand 1 Correspondence: Department of Pharmacology and Toxicology, University of Otago, P.O. Box 913, Dunedin, New Zealand. E-mail: ian.appleton@stonebow.otago.ac.nz <h3>SPECIFIC AIMS</h3> Hypoxia-ischemia (HI) -induced brain dysfunction, as well as other stroke-like syndromes, remains a growing concern with no current pharmacological treatment available. Spermine, a naturally occurring polyamine, has shown considerable promise as a putative neuroprotectant in models of neurodegeneration. To date, no study has used a model of HI-induced brain damage to assess the putative neuroprotective properties of spermine. More important, the mechanisms of this neuroprotective effect have not been determined. Therefore, in this study we used a modified Levine rat pup model (unilateral carotid artery ligation, coupled with global hypoxia) to evaluate the effects of various polyamines on HI-induced brain damage. In addition, we investigated the biochemical (NOS and arginase) and molecular energetics (mitochondrial complexes) in association with these effects. <h3>PRINCIPAL FINDINGS</h3> <h3>1. Spermine, but not putrescine or spermidine, provided gross histological neuroprotection</h3> H
/lp/fed-of-american-socs-for-experimental-biology/neuroprotective-effects-of-spermine-following-hypoxic-ischemic-induced-6YQjavV5Oe