研究论文

依达拉奉对脑缺血再灌注后Aβ及其前体表达干预

  • 任海燕 ,
  • 赵晖 ,
  • 王蕾 ,
  • 许晨波 ,
  • 马梅蕾 ,
  • 文娟
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  • 1. 新疆医科大学基础医学院, 乌鲁木齐830054;
    2. 首都医科大学中医药学院, 北京100054;
    3. 日本新潟药科大学临床药理学实验室, 东京956-8603
任海燕, 主治医师, 研究方向为神经病理生理学, 电子信箱:424732833@qq.com

收稿日期: 2015-01-14

  修回日期: 2015-04-21

  网络出版日期: 2015-07-15

基金资助

新疆维吾尔自治区自然科学基金项目(2011211A046)

Intervention of Edaravone on expression of β amyloid and amyloid precursor protein after cerebral ischemia reperfusion

  • REN Haiyan ,
  • ZHAO Hui ,
  • WANG Lei ,
  • XU Chenbo ,
  • MA Meilei ,
  • WEN Juan
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  • 1. School of Basic Medicine, Xinjiang Medical University, Urumqi 830054, China;
    2. School of Traditional Chinese Medicine, Capital Medical University, Beijing 100054, China;
    3. Laboratory of Clinical Pharmacology, Nigata University of Pharmacy and Applied Life Sciences, Tokyo 956-8603, Japan

Received date: 2015-01-14

  Revised date: 2015-04-21

  Online published: 2015-07-15

摘要

为探讨缺血再灌注对大鼠海马区神经元细胞的损伤机制及依达拉奉的干预作用, 利用大脑中动脉线栓法制备大鼠脑缺血再灌模型, 缺血2 h 后再灌注22 h(术后24 h), 按照Zea Longa 5 级评分法, 对大鼠进行神经行为学评分;通过苏木精-伊红染色法(HE)染色大鼠脑组织, 观察其病理形态学的改变;通过免疫组织化学, 图像分析及Western Blot 的方法检测大鼠海马区β淀粉样蛋白(Aβ)及其前体(APP)的表达。结果显示, 模型组大鼠表现出明显的神经功能缺损症状, 与之相比, 6 和10 mg/kg 的依达拉奉可不同程度改善损伤模型大鼠的神经缺损症状, 尤其是10 mg/kg 依达拉奉组的大鼠症状改善更为明显(P<0.01);HE 染色结果显示, 模型组大鼠海马区神经元细胞脱失明显, 而治疗组可减轻这种形态学改变;免疫组织化学及Western Blot 分析结果提示, 在模型组中Aβ、APP 表达明显高于假手术组(P<0.01), 而在不同质量分数依达拉奉组中, Aβ、APP 含量均减弱(P<0.05)。由此得出, 缺血再灌注可能通过上调淀粉样蛋白Aβ及其前体APP 而引起神经元细胞损伤, 而依达拉奉可能通过对它们的抑制起到保护神经元细胞的作用。

本文引用格式

任海燕 , 赵晖 , 王蕾 , 许晨波 , 马梅蕾 , 文娟 . 依达拉奉对脑缺血再灌注后Aβ及其前体表达干预[J]. 科技导报, 2015 , 33(12) : 77 -82 . DOI: 10.3981/j.issn.1000-7857.2015.12.013

Abstract

This paper investigates the damage mechanism of rat hippocampal neurons induced by the ischemia reperfusion and the intervention of the Edaravone. An ischemia reperfusion model is built by the middle cerebral artery occlusion (MACO)-reperfusion method. The reperfusion is performed 2 hours after the ischemia and persists for 22 hours (24 h since surgery). According to the Zea Longa's 5 level evaluation method, the neurobehavioral score of rats is graded; The rats' tissue pathological morphological changes are observed by the HE staining; the expressions of amyloid β (Aβ) and its precursor (APP) in the hippocampus of rats are detected with the immunohistochemistry, the image analysis and the Western Blot. It is shown that the model group rats show obvious symptoms of the nerve function defect; By contrast, the Edaravone of 6 and 10 mg/kg could improve model rats' symptoms of the nerve defect in varying degrees; And the difference is more significant in 10 mg/kg group (P<0.01). The HE staining shows that the depigmentation of the model group rat hippocampal neurons is obvious, and the two treatment groups could reduce this kind of morphology change; The immunohistochemistry and Western Blot analysis results suggest that both levels of Aβ and APP in the model group are significantly higher than those in the sham group (P<0.01), however, in different concentrations of Edaravone groups, their expression is significantly reduced (P<0.05). It is concluded that the ischemia reperfusion could cause neuron cells' damage by increasing Aβ and APP, and the Edaravone might suppress their toxic effects and protect the neuron cells by decreasing their expression.

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