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RESEARCH AND REPORT
Year : 2014  |  Volume : 9  |  Issue : 5  |  Page : 481-488

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


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

Correspondence Address:
M.D. Jiang Wu
Ph.D., Department of Neurology, the First Hospital of Jilin University, Changchun 130021, Jilin Province
China
M.D. Yu Yang
Ph.D. Department of Neurology, the First Hospital of Jilin University, Changchun 130021, Jilin Province
China
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Source of Support: Funding: 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., Conflict of Interest: None


DOI: 10.4103/1673-5374.130065

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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.


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