• L Beni-Adani, I Gozes, Y Cohen, Y Assaf, R A Steingart, D E Brenneman, O Eizenberg, V Trembolver, and E Shohami.
• Department of Neurosurgery, The Hebrew University Hadassah Medical Center, Jerusalem, Israel.
• J. Pharmacol. Exp. Ther. 2001 Jan 1;296(1):57-63.

AbstractBrain 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.

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