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

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

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

作者机构:Shanghai Key Laboratory of Orthopedic Implants Department of Orthopedic surgery Shanghai Ninth People's Hospital Shanghai Jiao Tong University School of Medicine Shanghai China 

出 版 物:《Neural Regeneration Research》 (中国神经再生研究(英文版))

年 卷 期:2017年第12卷第7期

页      面:1166-1171页

核心收录:

学科分类:1002[医学-临床医学] 100210[医学-外科学(含:普外、骨外、泌尿外、胸心外、神外、整形、烧伤、野战外)] 10[医学] 

基  金: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 

主  题:nerve regeneration spinal cord ischemia/reperfusion injury aldehyde dehydrogenase 2 alcohol apoptosis oxidative stress terminaldeoxynucleotidyl transferase dUTP nick-end labeling neural regeneration 

摘      要:Aldehyde dehydrogenase 2(ALDH2)is an important factor in inhibiting oxidative stress and has been shown to protect against renal ischemia/reperfusion ***,we hypothesized that ALDH_2 could reduce spinal cord ischemia/reperfusion *** cord ischemia/reperfusion injury was induced in rats using the modified Zivin's method of clamping the abdominal *** successful model establishment,the agonist group was administered a daily consumption of 2.5%*** 7 days post-surgery,the Basso,Beattie,and Bresnahan score significantly increased in the agonist group compared with the spinal cord ischemia/reperfusion injury ***_2expression also significantly increased and the number of apoptotic cells significantly decreased in the agonist group than in the spinal cord ischemia/reperfusion injury *** analysis revealed that ALDH_2 expression negatively correlated with the percentage of TUNEL-positive cells(r=-0.485,P〈0.01).In summary,increased ALDH_2 expression protected the rat spinal cord against ischemia/reperfusion injury by inhibiting apoptosis.

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