Open AccessrAAV/ABAD-DP-6His attenuates oxidative stress-induced injury of PC12 cells
Author(s) -
Mingyue Jia,
Mingyu Wang,
Yi Yang,
Yixin Chen,
Dujuan Liu,
Xu Wang,
Lei Song,
Jiang Wu,
Yang Yu
Publication year - 2014
Publication title -
neural regeneration research/neural regeneration research
Language(s) - Uncategorized
Resource type - Journals
SCImago Journal Rank - 0.93
H-Index - 38
eISSN - 1876-7958
pISSN - 1673-5374
DOI - 10.4103/1673-5374.130065
Subject(s) - oxidative stress , neuroprotection , malondialdehyde , superoxide dismutase , hydrogen peroxide , superoxide , reactive oxygen species , peptide , intracellular , decoy , apoptosis , pharmacology , chemistry , microbiology and biotechnology , biochemistry , medicine , biology , enzyme , receptor
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 Ca(2+) 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.