重组人血小板活化因子乙酰水解酶对大鼠脑梗死后缺血半暗带神经细胞超微结构的影响  

Effect of rPAF-AH on ultrastructure of neurons in ischemic penumbra of rats after cerebral infarction

作　　者：徐玉玲 王启征 黄蕾 曹裕民[1] 高玉元[1] 廖一夫 唐晓娜 张雄[1] Xu Yuling;Wang Qizheng;Huang Lei;Cao Yuming;Gao Yuyuan;Liao Yifu;Tang Xiaona;Zhang Xiong(Department of Neurology,Guangdong Provincial People's Hospital,Guangzhou 510080 ,Guangdong Province China)

机构地区：[1]广东省人民医院广东省神经科学研究所,广州510080 [2]汕头大学医学院

出　　处：《中华老年心脑血管病杂志》2019年第10期1080-1083,共4页Chinese Journal of Geriatric Heart,Brain and Vessel Diseases

基　　金：广东省科技计划项目(2013B021800193);广州市科技计划项目(201510010209)

摘　　要：目的从超微结构探讨重组人血小板活化因子乙酰水解酶(recombinant platelet-activating factor acetylhydrolase,rPAF-AH)对脑梗死大鼠缺血半暗带神经元的影响。方法将90只SD大鼠随机分为rPAF-AH组、生理盐水组和假手术组,每组30只。建立大鼠右侧大脑中动脉栓塞再灌注模型,在第2、7、14天进行神经行为学评分及透射电镜观察神经元细胞形态学改变。结果与生理盐水组比较,rPAF-AH组大鼠在第7天[(1.62±0.74)分vs (2.14±0.73)分,P<0.05]、第14天[(1.29±0.46)分vs (1.71±0.64)分,P<0.05]神经行为学评分均明显下降。透射电镜下生理盐水组可见神经细胞水肿,周围间隙增宽,细胞变形,染色质凝集,随着时间延长,神经元细胞不可逆损伤而逐渐凋亡,核内染色质松散甚至完全溶解;rPAF-AH组初期可见神经细胞明显水肿,但随着治疗时间延长,神经元细胞结构基本完整,可逆性损伤可逐渐改善。结论 rPAF-AH能有效改善大鼠脑梗死后神经功能缺损,可能与其缺血半暗带神经细胞超微结构保护作用有关。Objective To study the effect of recombinant platelet-activating factor acetylhydrolase (rPAF-AH) on ultrastructure of neurons in ischemic penumbra of rats after cerebral infarction. Methods Ninety SD rats were randomly divided into rPAF-AH group, acetylhydrolase group,normal saline group and sham operation group (30 in each group). A right middle cerebral artery embolism reperfusion model was established. The neurobehavior was scored and the morpholy of neurons was observed by transmission electron microscopy on days 2,7 and 14 before the animals were sacrified. Results The neurobehavioral score was significantly lower in rPAF-AH group than in normal saline group on days 7 and 14 before the animals were sacrified (1.62±0.74 vs 2.14± 0.73,P<0.05;1.29±0.46 -vs 1.71±0.64,P<0.05). Transmission electron microscopy showed edema, widened surrounding space, deformation, chromatin aggregation, irreversible damage and gradual apoptosis,loose or completely soluted chromatin of neurons in normal saline group. Edema of mitochondira,intact ultrastructure and reversible damage of neurons which was gradually improved with the time of treatment were detected in rPAF-AH group. Conclusion rPAF-AH can effectively improve the neurological deficit in rats after cerebral infarction, which is related with its protective effect on the ultrastructure of neurons in ischemic penumbra of rats.

关 键 词：血小板活化因子 1-烷基-2-乙酰甘油磷酸胆碱酯酶 脑梗死 再灌注 神经元 

分 类 号：R-332[医药卫生] R743.3