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抗坏血酸对减轻继发性脑损伤作用机制的研究
引用本文:张昊,茆翔,刘佰运.抗坏血酸对减轻继发性脑损伤作用机制的研究[J].安徽医药,2016,20(1):26-29.
作者姓名:张昊  茆翔  刘佰运
作者单位:中国人民武装警察部队总医院神经创伤科,北京 100039,中国人民武装警察部队总医院神经创伤科,北京 100039,中国人民武装警察部队总医院神经创伤科,北京 100039;首都医科大学附属北京天坛医院神经外科,北京 100050
基金项目:国家自然科学基金(No 81471238)
摘    要:目的 探讨抗坏血酸减轻颅脑创伤后继发性脑损伤加重的机制。方法 将实验大鼠随机分为假手术+生理盐水组、假手术+抗坏血酸组、打击+生理盐水组及打击+抗坏血酸组,每组 12 只。建立中度颅脑损伤模型,颅脑创伤后24 h进行神经功能损伤评分;采用酶联免疫吸附剂测定脑组织超氧化物歧化酶(SOD)活性;采用Western blot法测定颅脑创伤后24 h的损伤侧脑组织中细胞色素P450(CYP2E1),基质金属蛋白酶-9(MMP-9)和血脑屏障紧密连结蛋白Occludin的表达情况。结果 打击+抗坏血酸组的损伤程度与打击+生理盐水组相比明显减轻,SOD活力增高,CYP2E1表达减少,MMP-9的含量降低,Occludin的含量增高。结论 抗坏血酸可以通过降低血脑屏障的破坏程度,减轻继发性颅脑损伤的进一步加重,其作用可能是依靠抑制CYP2E1的表达而发挥的。

关 键 词:颅脑创伤  抗坏血酸  CYP2E1  氧化应激
收稿时间:2015/8/22 0:00:00
修稿时间:2015/11/27 0:00:00

Mechanisms of ascorbic acid reducing secondary brain injury in rats
ZHANG Hao,MAO Xiang and LIU Bai-yun.Mechanisms of ascorbic acid reducing secondary brain injury in rats[J].Anhui Medical and Pharmaceutical Journal,2016,20(1):26-29.
Authors:ZHANG Hao  MAO Xiang and LIU Bai-yun
Abstract:To investigate the effect of ascorbic acid on reducing secondary brain injury caused by traumatic brain injury and its possible mechanism.Methods Rats were randomly assigned into sham + saline group, sham + ascorbic acid group, hit + saline group and hit + ascorbic acid group, 12 in each group. Moderate traumatic brain injury model was established,and 24 hours later TBI neurological injury score was graded. The activity of superoxide dismutase in brain tissue was measured by ELISA. Western blot was used to determine the expressions of P450(CYP2E1), MMP-9 and Occludin in the tissue of the damaged brain 24 hours after the traumatic brain injury.Results Compared with the hit + saline group, in the blow + ascorbic acid group the trauma was significantly alleviated, the activity of SOD increased, the expression of CYP2E1 decreased, MMP-9 reduced and Occludin increased. Conclusions Ascorbic acid can alleviate the secondary brain injury by reducing the destruction of blood brain barrier, the mechanism of which is to inhibit the expression of CYP2E1.
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