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

• Main Authors: Xing-zhen Liu, Xin Sun, Kang-ping Shen, Wen-jie Jin, Zhi-yi Fu, Hai-rong Tao, Zhi-xing Xu
• Format: Article
• Language: English
• Published: Wolters Kluwer Medknow Publications 2017-01-01
• Series: Neural Regeneration Research
• Subjects: nerve regeneration; spinal cord ischemia/reperfusion injury; aldehyde dehydrogenase 2; alcohol; apoptosis; oxidative stress; terminal deoxynucleotidyl transferase dUTP nick-end labeling; neural regeneration
• Online Access: http://www.nrronline.org/article.asp?issn=1673-5374;year=2017;volume=12;issue=7;spage=1166;epage=1171;aulast=Liu

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.