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褪黑素对未成熟大鼠创伤性脑损伤所致脑氧化损伤的影响。

Effect of melatonin on brain oxidative damage induced by traumatic brain injury in immature rats.

作者信息

Ozdemir D, Uysal N, Gonenc S, Acikgoz O, Sonmez A, Topcu A, Ozdemir N, Duman M, Semin I, Ozkan H

机构信息

Department of Pediatrics, School of Medicine, Dokuz Eylul University, Inciralti, 35340, and Department of Neurosurgery, Ataturk Training and Research Hospital, Izmir, Turkey.

出版信息

Physiol Res. 2005;54(6):631-7.

PMID:15720160
Abstract

Progressive compromise of antioxidant defenses and free radical-mediated lipid peroxidation, which is one of the major mechanisms of secondary traumatic brain injury (TBI), has also been reported in pediatric head trauma. In the present study, we aimed to demonstrate the effect of melatonin, which is a potent free radical scavenger, on brain oxidative damage in 7-day-old rat pups subjected to contusion injury. Whereas TBI significantly increased thiobarbituric acid reactive substances (TBARS) levels, there was no compensatory increase in the antioxidant enzymes such as superoxide dismutase (SOD) and glutathione peroxidase (GPx) 24 hours after TBI in 7-day-old rats. Melatonin administered as a single dose of 5 mg/kg prevented the increase in TBARS levels in both non-traumatized and traumatized brain hemispheres. In conclusion, melatonin protects against oxidative damage induced by TBI in the immature brain.

摘要

抗氧化防御的渐进性损害以及自由基介导的脂质过氧化(这是继发性创伤性脑损伤(TBI)的主要机制之一)在小儿头部创伤中也有报道。在本研究中,我们旨在证明褪黑素(一种有效的自由基清除剂)对遭受挫伤性损伤的7日龄大鼠幼崽脑氧化损伤的影响。虽然TBI显著增加了硫代巴比妥酸反应性物质(TBARS)水平,但在7日龄大鼠TBI后24小时,超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GPx)等抗氧化酶没有代偿性增加。以5 mg/kg单剂量给药的褪黑素可防止未受伤和受伤脑半球的TBARS水平升高。总之,褪黑素可保护未成熟脑免受TBI诱导的氧化损伤。

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