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亚硒酸钠对沙土鼠海马CA1区神经元缺血/再灌注损伤的影响
引用本文:胡冬梅,李义召,王海涛,张秋玲,史中沂,张敬军,黄庆玉,聂斌. 亚硒酸钠对沙土鼠海马CA1区神经元缺血/再灌注损伤的影响[J]. 中国药理学通报, 2007, 23(2): 268-271
作者姓名:胡冬梅  李义召  王海涛  张秋玲  史中沂  张敬军  黄庆玉  聂斌
作者单位:1. 泰山医学院附属医院神经内科,山东,泰安,271000
2. 长城医院,山东,济南,250000
3. 泰山医学院机能实验室,山东,泰安,271000
4. 泰山医学院病理教研室,山东,泰安,271000
5. 泰山医学院信息科学系,山东,泰安,271000
摘    要:目的探讨亚硒酸钠对沙土鼠海马CA1区神经元缺血/再灌注损伤的影响。方法采用夹闭双侧颈动脉法制备沙土鼠前脑缺血/再灌注模型,双重染色,电镜下观察各组海马CA1区神经元的超微结构变化。TUNEL染色光镜下观察和计数凋亡神经元,计算凋亡密度。结果硒处理组沙土鼠脑缺血/再灌注后,神经元超微结构的病理形态损伤减轻,凋亡细胞减少,与对照组比较差异有显著性(P<0.01)。结论亚硒酸钠对沙土鼠脑缺血/再灌注损伤的海马CA1区神经元超微结构及凋亡细胞具有保护作用。

关 键 词:缺血/再灌注损伤  亚硒酸钠  超微结构  凋亡
文章编号:1001-1978(2007)02-0268-04
修稿时间:2006-09-20

Effects of sodium selenite on neurons of hippocampus CA1 of cerebral ischemic-reperfused injury in gerbils
HU Dong-mei,LI Yi-zhao,WANG Hai-tao,ZHANG Qiu-ling,SHI Zhong-yi,ZHANG Jing-jun,HUANG Qing-yu,NIE Bin. Effects of sodium selenite on neurons of hippocampus CA1 of cerebral ischemic-reperfused injury in gerbils[J]. Chinese Pharmacological Bulletin, 2007, 23(2): 268-271
Authors:HU Dong-mei  LI Yi-zhao  WANG Hai-tao  ZHANG Qiu-ling  SHI Zhong-yi  ZHANG Jing-jun  HUANG Qing-yu  NIE Bin
Abstract:Aim To study effects of sodium selenite on neurons of hippocampus CA1 of cerebral ischemic-reperfused injury in gerbils. Methods 40 gerbils were randomly divided into five groups:Ⅰ:sham-operated group;Ⅱ-Ⅲ:cerebral ischemic reperfusion group for 2 days and 4 days; Ⅳ-Ⅴ:cerebral ischemic reperfusion for 2 days and 4 days with sodium selenite-treated group. Clipping bilateral common carotid arteries after five minutes in all groups except the sham-operated group. Ultrastructure changes of hippocampus were observed by electron microscope. Apoptosis was observed by the TUNEL method, the number of apoptosis cells was counted and density was calculated. Results The pathological changes of hippocampus CA1 were lighter, the number of apoptosis cells was low (P<0.01). Conclusion Sodium selenite could protect neurons against cerebral ischemic reperfusion injure.
Keywords:cerebral ischemic reperfusion injury  sodium selenite  ultrastructure  apoptosis
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