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/ABADDP-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. However, whether it improves oxidative stress injury remains unclear. In this study, a recombinant adenovirus constitutively secreting and expressing A [beta] -binding alcohol dehydrogenase (ABAD) decoy peptide antagonizes A [beta] ABAD decoy peptide (rAAV / ABAD-DP-6His) was successfully constructed. Our results was that of rAAV / ABAD-DP-6His increased superoxide dismutase activity in hydrogen peroxide-induced oxidative stress-mediated injury of PC12 cells. -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 was 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 ind uced by hydrogen peroxide, thus exerting neuroprotective effects.