Fucoxanthin prevents H2O2-induced neuronal apoptosis via concurrently activating the PI3-K/Akt cascade and inhibiting the ERK pathway
Background : As a natural carotenoid abundant in chloroplasts of edible brown algae, fucoxanthin possesses various health benefits, including anti-oxidative activity in particular.
Objective : In the present study, we studied whether fucoxanthin protected against hydrogen peroxide (H 2 O 2 )-induced neuronal apoptosis.
Design : The neuroprotective effects of fucoxanthin on H 2 O 2 -induced toxicity were studied in both SH-SY5Y cells and primary cerebellar granule neurons.
Results : Fucoxanthin significantly protected against H 2 O 2 -induced neuronal apoptosis and intracellular reactive oxygen species. H 2 O 2 treatment led to the reduced activity of phosphoinositide 3-kinase (PI3-K)/Akt cascade and the increased activity of extracellular signal-regulated kinase (ERK) pathway in SH-SY5Y cells. Moreover, fucoxanthin significantly restored the altered activities of PI3-K/Akt and ERK pathways induced by H 2 O 2 . Both specific inhibitors of glycogen synthase kinase 3β (GSK3β) and mitogen-activated protein kinase kinase (MEK) significantly protected against H 2 O 2 -induced neuronal death. Furthermore, the neuroprotective effects of fucoxanthin against H 2 O 2 -induced neuronal death were abolished by specific PI3-K inhibitors.
Conclusions : Our data strongly revealed that fucoxanthin protected against H 2 O 2 -induced neurotoxicity via concurrently activating the PI3-K/Akt cascade and inhibiting the ERK pathway, providing support for the use of fucoxanthin to treat neurodegenerative disorders induced by oxidative stress.
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