We evaluated the antioxidant activity and neuronal cell-protective effect of fucoidan extract from Ecklonia cava (FEC) on hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>)-induced cytotoxicity in PC-12 and MCIXC cells to assess it...
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https://www.riss.kr/link?id=A105090785
2018
Korean
SCIE,SCOPUS,KCI등재
학술저널
40-49(10쪽)
0
상세조회0
다운로드다국어 초록 (Multilingual Abstract)
We evaluated the antioxidant activity and neuronal cell-protective effect of fucoidan extract from Ecklonia cava (FEC) on hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>)-induced cytotoxicity in PC-12 and MCIXC cells to assess it...
We evaluated the antioxidant activity and neuronal cell-protective effect of fucoidan extract from Ecklonia cava (FEC) on hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>)-induced cytotoxicity in PC-12 and MCIXC cells to assess its protective effect against oxidative stress. Antioxidant activities were examined using the ABTS radical scavenging activity and malondialdehyde-inhibitory effect, and the results showed that FEC had significant antioxidant activity. Intracellular ROS contents and neuronal cell viability were investigated using the DCF-DA assay and MTT reduction assay. FEC also showed remarkable neuronal cell-protective effect compared with vitamin C as a positive control for both H<sub>2</sub>O<sub>2</sub>-treated PC-12 and MC-IXC cells. Based on the neuronal cellprotective effects, mitochondrial function was analyzed in PC-12 cells, and FEC significantly restored mitochondrial damage by increasing the mitochondrial membrane potential (Δψm) and ATP levels and regulating mitochondrial-mediated proteins (p-AMPK and BAX). Finally, the inhibitory effects against acetylcholinesterase (AChE), which is a critical hydrolyzing enzyme of the neurotransmitter acetylcholine in the cholinergic system, were investigated (IC<sub>50</sub> value = 1.3 mg/ml) and showed a mixed (competitive and noncompetitive) pattern of inhibition. Our findings suggest that FEC may be used as a potential material for alleviating oxidative stress-induced neuronal damage by regulating mitochondrial function and AChE inhibition.