摘要
目的 探讨急性乙醇中毒对大鼠颅脑创伤后神经系统的影响及其氧自由基损伤机制.方法 Feeney法制作大鼠重型颅脑损伤模型,乙醇灌胃法建立急性乙醇中毒模型.48只雄性SD大鼠随机分为单纯急性乙醇中毒组（A组）、单纯颅脑创伤组（B组）、急性乙醇中毒合并颅脑创伤组（C组）和假手术组（D组）各12只.在伤后1、6、24、72h进行行为学评分;在伤后72h,各组随机取其中6只在麻醉下经心脏灌注4%多聚甲醛固定脑组织,TUNEL法测凋亡细胞数;其余6只快速断头取水肿带脑组织,测定脑组织内SOD活性及MDA含量.结果 C组大鼠的行为学评分最低,恢复最慢;其脑组织内MDA含量最高,SOD含量最低;其神经细胞凋亡最多.结论 急性乙醇中毒可加重颅脑创伤后氧自由基的损害,增加神经细胞的凋亡,影响神经功能的恢复.
Objective To investigate the influence of acute ethanol intoxication （AEI） on traumatic brain injury （TBI） in rats and its relation to oxygen free radicals. Methods Severe traumatic brain injury model was established by Feeny method in rats, and acute ethanol intoxication was induced by gastric gavage. Forty-eight male SD rats were randomly divided into 4 groups： acute ethanol intoxication group （A）, traumatic brain injury group （B）, acute ethanol intoxication with traumatic brain injury group （C） and sham operation group （D）. The behavioral scores were examined at lh, 6h, 24h and 72h after injury. After 72h, 6 rats from each group were sacrificed and brain specimens were collected. The apoptotic cells were detected by TUNEL method; the superoxide dismutase （SOD） and malondialdehyde （MDA） were determined. Data were analyzed by one-way ANOVA. Results The behavior score of group C was the lowest （P〈0.05） and delayed to recover （P〈0.05）. In group C the content of MDA was the highest and SOD was the lowest （P〈0.05）; the percentage of apoptosis cells was the highest among 4 groups （P〈0.05）. Conclusion Acute ethanol intoxication exacerbates oxygen free radical damage after traumatic brain injury, increases neural cell apoptosis and affects the recovery of neurological function
出处
《浙江医学》
CAS
2011年第5期622-625,共4页
Zhejiang Medical Journal
基金
宁波市自然科学基金资助项目（2010A610065）
慈溪市科技局资助项目（CN2008032,CN2009022）
关键词
急性乙醇中毒
颅脑创伤
超氧化物歧化酶
丙二醛
细胞凋亡
Acute ethanol intoxication Traumatic brain injury Superoxide dismutase Malondialdehyde Apoptosis
