[1]赵雅宁,李建民,刘乐,等.内质网应激相关分子GRP78在高血压加重全脑缺血大鼠神经损伤中的作用[J].南方医科大学学报,2012,(11):1675.
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内质网应激相关分子GRP78在高血压加重全脑缺血大鼠神经损伤中的作用()
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《南方医科大学学报》[ISSN:1673-4254/CN:44-1627/R]

卷:
期数:
2012年11期
页码:
1675
栏目:
出版日期:
2012-11-15

文章信息/Info

作者:
赵雅宁李建民刘乐常学优陈长香李淑杏
关键词:
高血压脑缺血再灌注葡萄糖调节蛋白78内质网应激
摘要:
目的观察常态大鼠和自发性高血压大鼠全脑缺血再灌注后海马区葡萄糖调节蛋白78(GRP78)表达变化,探讨其在高血
压增加脑缺血再灌注神经易损性中的可能意义。方法60只雄性Wistar-Kyoto(WKY)大鼠随机分为假手术组和全脑缺血再灌
注组;另取30只雄性自发性高血压大鼠为高血压全脑缺血再灌注组。采用改良的Pulsineli4血管阻断(4-VO)法制作全脑缺血
再灌注模型。应用苏木伊红染色观察海马区神经细胞形态变化;免疫组织化学法和免疫印迹法检测海马区GRP78表达;八臂迷
宫检测动物行为学变化。结果与假手术组比较,全脑缺血再灌注组存活神经细胞密度降低;GRP78表达增高,24h达高峰,与
脑缺血再灌注组比较,高血压全脑缺血组各时间点存活神经细胞密度降低;GRP78表达6h增高,24、48h持续减少;动物行为学
评分与全脑缺血组差异显著。结论高血压加重脑缺血再灌注神经损伤,其机制与下降GRP78表达、增加神经细胞丢失有关。

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更新日期/Last Update: 1900-01-01