A peptide derived from activity-dependent neuroprotective protein (ADNP) ameliorates injury response in closed head injury in mice

被引:0
|
作者
Beni-Adani, L
Gozes, I
Cohen, Y
Assaf, Y
Steingart, RA
Brenneman, DE
Eizenberg, O
Trembolver, V
Shohami, E [1 ]
机构
[1] Hebrew Univ Jerusalem, Sch Pharm, Dept Pharmacol, Hadassah Med Ctr, IL-91120 Jerusalem, Israel
[2] Hebrew Univ Jerusalem, Hadassah Med Ctr, Dept Neurosurg, IL-91120 Jerusalem, Israel
[3] Tel Aviv Univ, Sackler Fac Exact Sci, Sch Chem, IL-69978 Tel Aviv, Israel
[4] Tel Aviv Univ, Sackler Fac Med, Dept Clin Biochem, IL-69978 Tel Aviv, Israel
[5] NICHD, Sect Dev & Mol Pharmacol, Dev Neurobiol Lab, NIH, Bethesda, MD USA
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中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
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.
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页码:57 / 63
页数:7
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