Neuroprotective effect of edible brown alga Eisenia bicyclis on amyloid beta peptide-induced toxicity in PC12 cells

Amyloid beta peptide (A beta) oligomers increase intracellular reactive oxygen species (ROS) and calcium cation (Ca2+) concentrations, which causes neuronal cell death in Alzheimer's disease (AD). Thus, the use of neuroprotective agents with antioxidative activity might be effective in the treatment of AD. In the present study, the neuroprotective effects of the methanol extract from edible brown alga Eisenia bicyclis (Laminariaceae) and its solvent soluble fractions together with the isolated phlorotannins on A beta-induced toxicity were assessed by cell viability, intracellular ROS, and Ca2+ levels in PC12 cells. The addition of the methanol extract as well as its ethyl acetate and n-butanol fractions of E. bicyclis markedly reversed the A beta-induced toxicity. Among six phlorotannins, including phloroglucinol (1), dioxinodehydroeckol (2), eckol (3), phlorofucofuroeckol A (4), dieckol (5), and 7-phloroeckol (6), isolated from the most active ethyl acetate fraction, 3-6 significantly decreased A beta-induced cell death. Furthermore, these compounds also inhibited intracellular ROS generation and Ca2+ generation, indicating the neuroprotective effects may be mediated through reduced intracellular ROS and Ca2+ generation. Thus, the results of the present study imply that E. bicyclis and its active components attenuated the oxidative stress and reduced neuronal cell death, suggesting that it may be used as a dietary neuroprotective agent in AD.