Neural Regeneration Research ›› 2017, Vol. 12 ›› Issue (7): 1166-1171.doi: 10.4103/1673-5374.211198

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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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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