Neural Regeneration Research ›› 2014, Vol. 9 ›› Issue (5): 481-488.doi: 10.4103/1673-5374.130065

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rAAV/ABAD-DP-6His attenuates oxidative stress-induced injury of PC12 cells

Mingyue Jia 1, Mingyu Wang  2, Yi Yang 1, Yixin Chen 3, Dujuan Liu 4, Xu Wang 1, Lei Song 1, Jiang Wu 1, Yu Yang 1   

  1. 1 Department of Neurology, the First Hospital of Jilin University, Changchun, Jilin Province, China
    2 Department of Neurology, People’s Hospital of Jilin Province, Changchun, Jilin Province, China
    3 Radioactive Medicine Specialty, College of Public Health in Jilin University, Changchun, Jilin Province, China
    4 Department of Burn and Plastic Surgery, the General Hospital of CNPC in Jilin, Jilin, Jilin Province, China
  • Received:2014-02-16 Online:2014-03-12 Published:2014-03-12
  • Contact: Jiang Wu, M.D., Ph.D., Department of Neurology, the First Hospital of Jilin University, Changchun 130021, Jilin Province, China, wujiang 540214@126.com. Yu Yang, M.D., Ph.D., Department of Neurology, the First Hospital of Jilin University, Changchun 130021, Jilin Province, China, yy197711@yahoo.com.cn.
  • Supported by:

    This study was supported by the National Natural Science Foundation of China for the Youth, No. 30800338, 30801211; the National Natural Science Foundation of China, No. 30872721.

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Abstract:

Our previous studies have revealed that amyloid β (Aβ)-binding alcohol dehydrogenase (ABAD) decoy peptide antagonizes Aβ42-induced neurotoxicity. However, whether it improves oxidative stress injury remains unclear. In this study, a recombinant adenovirus constitutively secreting and expressing Aβ-ABAD decoy peptide (rAAV/ABAD-DP-6His) was successfully constructed. Our results showed that rAAV/ABAD-DP-6His increased superoxide dismutase activity in hydrogen peroxide-induced oxidative stress-mediated injury of PC12 cells. Moreover, rAAV/ABAD-DP-6His decreased malondialdehyde content, intracellular Ca2+ concentration, and the level of reactive oxygen species. rAAV/ABAD-DP-6His maintained the stability of the mitochondrial membrane potential. In addition, the ATP level remained constant, and apoptosis was reduced. Overall, the results indicate that rAAV/ABAD-DP-6His generates the fusion peptide, Aβ-ABAD decoy peptide, which effectively protects PC12 cells from oxidative stress injury induced by hydrogen peroxide, thus exerting neuroprotective effects.

Key words: nerve regeneration, neurodegenerative disease, gene therapy, Alzheimer’s disease, amyloid beta peptide, amyloid beta binding alcohol dehydrogenase, adeno-associated virus, hydrogen peroxide, oxidative stress, mitochondrial dysfunction, NSFC grant, neural regeneration