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p66Shc基因敲除对小鼠缺血缺氧性脑损伤的保护作用

孔祥溢 关健 王任直

孔祥溢, 关健, 王任直. p66Shc基因敲除对小鼠缺血缺氧性脑损伤的保护作用[J]. 协和医学杂志, 2017, 8(6): 359-363. doi: 10.3969/j.issn.1674-9081.2017.06.008
引用本文: 孔祥溢, 关健, 王任直. p66Shc基因敲除对小鼠缺血缺氧性脑损伤的保护作用[J]. 协和医学杂志, 2017, 8(6): 359-363. doi: 10.3969/j.issn.1674-9081.2017.06.008
Xiang-yi KONG, Jian GUAN, Ren-zhi WANG. Neuroprotective Effects of p66Shc Knock-out on Hypoxic-ischemic Brain Injury in Mice[J]. Medical Journal of Peking Union Medical College Hospital, 2017, 8(6): 359-363. doi: 10.3969/j.issn.1674-9081.2017.06.008
Citation: Xiang-yi KONG, Jian GUAN, Ren-zhi WANG. Neuroprotective Effects of p66Shc Knock-out on Hypoxic-ischemic Brain Injury in Mice[J]. Medical Journal of Peking Union Medical College Hospital, 2017, 8(6): 359-363. doi: 10.3969/j.issn.1674-9081.2017.06.008

p66Shc基因敲除对小鼠缺血缺氧性脑损伤的保护作用

doi: 10.3969/j.issn.1674-9081.2017.06.008
详细信息
    通讯作者:

    王任直 电话:010-69152530, E-mail:wrzpumch@163.com

  • 中图分类号: R651.1+2

Neuroprotective Effects of p66Shc Knock-out on Hypoxic-ischemic Brain Injury in Mice

More Information
    Corresponding author: WANG Ren-zhi Tel: 010-69152530, E-mail: wrzpumch@163.com
  • 摘要:   目的  探讨p66Shc基因敲除对小鼠缺血缺氧性脑损伤(hypoxic-ischemic brain injury, HIBI)的保护作用及可能的机理。  方法  将C57小鼠分为假手术组(野生型, sham operation, SO)、HIBI野生型组(hypoxic-ischemic wild type, HIWT)和HIBI-p66Shc基因敲除组(hypoxic-ischemic knock-out, HIKO), 每组20只。采用右侧颈总动脉结扎-浸入低氧环境的方法制备小鼠HIBI模型。随后对各组小鼠神经功能障碍情况、HIBI损伤灶体积、血清神经元特异性烯醇化酶(neuronspecific enolase, NSE)水平和脑组织匀浆中白细胞介素-1β(interleukin-1β, IL-1β)的水平进行测量和比对。  结果  HIBI造模24 h后, HIKO组小鼠的神经功能缺损程度评分(1.87±0.30)低于HIWT组小鼠(2.49±0.26), HIKO组小鼠脑梗死灶体积[(22.66±4.20)mm3]小于HIWT组小鼠[(27.31±3.23)mm3], HIKO组小鼠血清NSE含量[(8.97±0.74)ng/ml]显著低于HIWT组小鼠[(11.26±0.68)ng/ml], HIKO组小鼠脑组织IL-1β含量[(1.72±0.30)ng/ml]显著低于HIWT组小鼠[(2.07±0.28)ng/ml], P均 < 0.05。  结论  p66Shc基因敲除可通过降低小鼠HIBI发生后脑组织IL-1β的表达, 起到脑保护作用。
  • 图  1  HIBI-p66Shc基因敲除组(A)和HIBI野生型组(B)脑梗死灶免疫组织化学染色(×20)

    HIBI:缺血缺氧性脑损伤

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出版历程
  • 收稿日期:  2017-06-12
  • 刊出日期:  2017-11-30

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