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Vol. 296, Issue 1, 57-63, January 2001

A Peptide Derived from Activity-Dependent Neuroprotective Protein (ADNP) Ameliorates Injury Response in Closed Head Injury in Mice

Liana Beni-Adani, Illana Gozes, Yoram Cohen, Yaniv Assaf, Ruth A. Steingart, Douglas E. Brenneman, Oded Eizenberg, Victoria Trembolver and Esther Shohami

Departments of Neurosurgery (L.B.-A., O.E.) and Pharmacology (V.T., E.S.), The Hebrew University Hadassah Medical Center, Jerusalem, Israel; Clinical Biochemistry, Sackler Faculty of Medicine (R.A.S., I.G.), School of Chemistry, Sackler Faculty of Exact Sciences (Y.C., Y.A.), Tel Aviv University, Tel Aviv, Israel; and Section on Developmental and Molecular Pharmacology, Laboratory of Developmental Neurobiology, National Institute of Child and Human Development, National Institutes of Health, Bethesda, Maryland (D.E.B.)

Brain injury induces disruption of the blood-brain barrier, edema, and release of autodestructive factors that produce delayed neuronal damage. NAPSVIPQ (NAP), a femtomolar-acting peptide, is shown to be neuroprotective in a mouse model of closed head injury. NAP injection after injury reduced mortality and facilitated neurobehavioral recovery (P < 0.005). Edema was reduced by 70% in the NAP-treated mice (P < 0.01). Furthermore, in vivo magnetic resonance imaging demonstrated significant brain-tissue recovery in the NAP-treated animals. NAP treatment decreased tumor necrosis factor-alpha levels in the injured brain and was shown to protect pheochromocytoma (PC12 cells) against tumor necrosis factor-alpha -induced toxicity. Thus, NAP provides significant amelioration from the complex array of injuries elicited by head trauma.

0022-3565/01/2961-0057$03.00/0
THE JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS
Copyright © 2001 by The American Society for Pharmacology and Experimental Therapeutics


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