A peptide derived from activity-dependent neuroprotective protein (ADNP) ameliorates injury response in closed head injury in mice.
A peptide derived from activity-dependent neuroprotective protein (ADNP) ameliorates injury response in closed head injury in mice.
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发表时间：
2001
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通讯作者：
L. Beni‐Adani;I. Gozes;Y. Cohen;Y. Assaf;R. Steingart;D. Brenneman;O. Eizenberg;V. Trembolver;E. Shohami
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作者：
L. Beni‐Adani;I. Gozes;Y. Cohen;Y. Assaf;R. Steingart;D. Brenneman;O. Eizenberg;V. Trembolver;E. Shohami
脑损伤引起血脑屏障的破坏、水肿和产生迟发性神经元损伤的自身破坏因子的释放。NAPSVIPQ（NAP）是一种飞秒作用肽，在闭合性头部损伤的小鼠模型中显示出神经保护作用。损伤后注射NAP可降低死亡率，促进神经行为恢复（P < 0.005）。经NAP处理的小鼠水肿减轻了70%（P < 0.01）。此外，体内磁共振成像显示NAP治疗动物的脑组织恢复显著。NAP治疗降低了受损脑中的肿瘤坏死因子-α水平，并显示出保护嗜铬细胞瘤（PC 12细胞）免受肿瘤坏死因子-α诱导的毒性。因此，NAP提供了从由头部创伤引起的一系列复杂损伤的显著改善。
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.