RAAV/ABAD-DP-6His generates fusion peptide that protects PC12 cells from oxidative stress injury

The effects of Amyloid beta (Aβ)-Aβ-binding alcohol dehydrogenase (ABAD) may exacerbate Alzheimer's disease pathology. Therefore, blocking Aβ-ABAD-mediate effects with ABAD decoy peptide (ABAD-DP) may be a potential therapeutic strategy for Alzheimer's disease. Dr. Jiang Wu and team from the First Hospital of Jilin University in China successfully constructed a recombinant adenovirus constitutively secreting and expressing Aβ-ABAD decoy peptide (rAAV/ABAD-DP-6His). Their 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 experimental findings, published in the Neural Regeneration Research (Vol. 9, No. 5, 2014), 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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