中国神经再生研究(英文版)

中国神经再生研究(英文版) ›› 2017, Vol. 12 ›› Issue (7): 1166-1171.doi: 10.4103/1673-5374.211198

• 原著:脊髓损伤修复保护与再生 • 上一篇    下一篇

乙醛脱氢酶2过表达抑制脊髓缺血再灌注损伤后的神经元凋亡

  

  • 收稿日期:2017-04-22 出版日期:2017-07-15 发布日期:2017-07-15
  • 基金资助:

    上海第九人民医院自然基金研究项目(syz2014-014).

Aldehyde dehydrogenase 2 overexpression inhibits neuronal apoptosis after spinal cord ischemia/ reperfusion injury

Xing-zhen Liu, Xin Sun, Kang-ping Shen, Wen-jie Jin, Zhi-yi Fu, Hai-rong Tao, Zhi-xing Xu   

  1. Shanghai Key Laboratory of Orthopedic Implants, Department of Orthopedic Surgery, Shanghai Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China
  • Received:2017-04-22 Online:2017-07-15 Published:2017-07-15
  • Contact: Kang-ping Shen, M.D. or Wen-jie Jin, M.D., shkp2016@163.com or surgeonjin@126.com.
  • Supported by:

    This research was supported by the Natural Science Research Fund Project of Shanghai Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine of China, No. syz2014-014.

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摘要：

有研究发现乙醛脱氢酶2是体内重要的抗氧化应激的保护因子，可减轻大鼠肾缺血再灌注损伤。为此，实验假设乙醛脱氢酶2过表达可减轻脊髓缺血再灌注损伤。采用Zivin改良法夹闭腹主动脉建立脊髓缺血再灌注损伤模型大鼠，造模成功后给予脊髓缺血再灌注损伤模型大鼠乙醛脱氢酶2激动剂-乙醇(2.5%)日常饮用。术后7 d见大鼠BBB评分明显增高；L2-5脊髓组织乙醛脱氢酶2蛋白表达明显增高，L2-5脊髓组织损伤程度明显减轻，凋亡细胞数明显减少；相关性分析显示乙醛脱氢酶2蛋白表达和细胞凋亡率变化呈明显负相关(r= -0.485, P < 0.01)。结果证实乙醛脱氢酶2过表达可抑制脊髓缺血再灌注损伤后的神经元凋亡，发挥对损伤脊髓的神经保护作用。

ORCID:0000-0003-4355-3142(Kang-ping Shen); 0000-0002-5521-7341(Wen-jie Jin)

关键词: 神经再生, 脊髓缺血再灌注损伤, 乙醛脱氢酶2, 乙醇, 细胞凋亡, 氧化应激, TUNEL

Abstract:

Aldehyde dehydrogenase 2 (ALDH2) is an important factor in inhibiting oxidative stress and has been shown to protect against renal ischemia/reperfusion injury. Therefore, we hypothesized that ALDH2 could reduce spinal cord ischemia/reperfusion injury. Spinal cord ischemia/reperfusion injury was induced in rats using the modified Zivin’s method of clamping the abdominal aorta. After successful model establishment, the agonist group was administered a daily consumption of 2.5% alcohol. At 7 days post-surgery, the Basso, Beattie, and Bresnahan score significantly increased in the agonist group compared with the spinal cord ischemia/reperfusion injury group. ALDH2 expression also significantly increased and the number of apoptotic cells significantly decreased in the agonist group than in the spinal cord ischemia/reperfusion injury group. Correlation analysis revealed that ALDH2 expression negatively correlated with the percentage of TUNEL-positive cells (r = −0.485, P < 0.01). In summary, increased ALDH2 expression protected the rat spinal cord against ischemia/reperfusion injury by inhibiting apoptosis.

Key words: nerve regeneration, spinal cord ischemia/reperfusion injury, aldehyde dehydrogenase 2, alcohol, apoptosis, oxidative stress, terminal deoxynucleotidyl transferase dUTP nick-end labeling, neural regeneration