Alzheimer's disease (AD) is a neurodegenerative disorder characterized by selective neuron loss, amyloid
plaques, and neurofibrillary tangles. Oxidative stress plays an essential role in the progression of AD. As the carotenoid
crocetin has been shown to possess anti-oxidative effects in previous studies, now we have investigated the
neuroprotective effects and potential molecular mechanism of crocetin action against Aβ1-42 induced toxicity in mouse
hippocampal-derived Ht22 cells. Our results showed that there was a significant reduction in Ht22 cell viability when
exposed to Aβ1-42 (0.5 µM) for 24 hours. Furthermore, increased reactive oxygen species production, reduced
mitochondrial membrane potential and phosphorylation of extracellular signal-regulated kinase were observed in the cells.
However, when pre-incubated with crocetin (1 and 5 µM) for 24 hours followed by Aβ1-42 (0.5 µM) challenge, there was a
marked increase in cell viability, reduced in reactive oxygen species formation, and increased mitochondrial membrane
potential. Pre-treatment with crocetin (5 µM) also activated extracellular signal-regulated kinase 1/2 phosphorylation.
These data demonstrate that crocetin has neuroprotective effects on Aβ1-42-induced Ht22 cell injury which may result from
its anti-oxidative role. This finding may provide a potential therapeutic candidate for the treatment of AD.
Keywords: Alzheimer's disease, β-amyloid (1-42), crocetin, Ht22, oxidative stress.
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