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作 者:黄慧玲[1] 刘锐[1] 王琴[1] 莫丽冬[1] 梁建伟[1]
机构地区:[1]天津市环湖医院、天津市神经外科研究所,300060
出 处:《天津医药》2008年第6期438-440,共3页Tianjin Medical Journal
基 金:国家“973”计划子课题(项目编号:2005CB522604);天津市“211”“重中之重”学科建设专项基金资助项目(项目编号:05YFGDSF02500)
摘 要:目的:研究亚低温治疗对颅脑创伤(TBI)大鼠线粒体活性氧(ROS)生成和ATP酶合成能力的影响。方法:72只动物随机分为假手术组、常温TBI组(肛温36℃~37℃)、亚低温TBI组(肛温31℃~33℃,亚低温持续2h),后2组利用液压打击(FPI)制作中度TBI模型。各组于脑外伤后2h,24h,3d和7d断头取伤侧大脑组织,差速离心法提取伤侧脑线粒体,酶荧光法检测线粒体ATP合成能力,荧光法测定线粒体ROS的生成。结果:常温TBI组脑创伤后线粒体ATP合成能力显著下降,24h降至最低,至7d时仍显著低于假手术组,ROS在各时间点均显著升高,3d时为最高。亚低温TBI组线粒体ATP合成能力在各时间点均高于常温TBI组,除2h外,其他时间点ROS低于常温TBI组。结论:颅脑创伤后线粒体ATP合成能力显著下降,ROS显著升高,亚低温可以改善线粒体ATP酶合成能力,抑制活性氧大量生成,从而保护脑组织。Objective: To study the effect of moderate hypothermia on cerebral mitochondrial reactive oxygen species (ROS) and ATP synthesis in with traumatic brain injury (TBI). Methods: Seventy-two rats were randomly divided into 3 groups which included sham(uninjured ) control group, normothermic TBI group(37 ℃ ) and moderate hypothermic TBI group (31 ℃-32 ℃, 2 h ). The moderate TBI model was founded with FPI. The ipsilateral brain was dissected and homogenized brain tissue was extracted to obtain mitochondria by density-centrifugation and speed-centrifugation 2 h,24 h,3 d,and 7 d after TBI. ROS and capacity of ATP synthesis were tested by fluorescent method. Results: The capacity of ATP synthesis in TBI group decreased,reached the lowest at 24 hours,and still lower than that in sham group 7 days after injury. ROS increased remarkably after TBI,and got highest level at 3 days. The capacity of ATP synthesis increased in hypothermia group than that in normothermic TBI group (P 〈 0.01 ), and ROS decreased than that in normothermie TBI group except 24 hours (P 〈 0.01). Conclusion: Hypothermia can take the protection of brain tissue after TBI by improving the capacity of ATP and inhibiting ROS production of the cerebral mitochondria.
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