Effect of Astaxanthin on Tissue Transglutaminase and Cytoskeletal Protein Expression in Amyloid-Beta Stressed Olfactory Ensheathing Cells: Molecular and Delayed Luminescence Studies

Astaxanthin, a natural compound of Haematococcus pluvialis, possesses antioxidant, antiinflammatory, anti-tumor and immunomodulatory activities. It also represents a potential therapeuticin Alzheimer's disease (AD), that is related to oxidative stress and agglomeration of proteins suchas amyloid-beta (A?). A? is a neurotoxic protein and a substrate of tissue transglutaminase (TG2),an ubiquitary protein involved in AD. Herein, the effect of astaxanthin pretreatment on olfactoryensheathing cells (OECs) exposed to A?(1-42) or by A?(25-35) or A?(35-25), and on TG2 expressionwere assessed. Vimentin, GFAP, nestin, cyclin D1 and caspase-3 were evaluated. ROS levels and thepercentage of cell viability were also detected. In parallel, delayed luminescence (DL) was used tomonitor mitochondrial status. ASTA reduced TG2, GFAP and vimentin overexpression, inhibitingcyclin D1levels and apoptotic pathway activation which induced an increase in the nestin levels.In addition, significant changes in DL intensities were particularly observed in OECs exposed toA? toxic fragment (25-35), that completely disappear when OECs were pre-incubated in astaxantin.Therefore, we suggest that ASTA pre-treatment might represent an innovative mechanism to contrastTG2 overexpression in AD.