Protective Effect of Fucoidan Extract from Ecklonia cava on Hydrogen Peroxide-Induced Neurotoxicity
- Authors
- Park, Seon Kyeong; Kang, Jin Yong; Kim, Jong Min; Park, Sang Hyun; Kwon, Bong Seok; Kim, Gun-Hee; Heo, Ho Jin
- Issue Date
- Jan-2018
- Publisher
- 한국미생물·생명공학회
- Keywords
- Ecklonia cava; fucoidan; oxidative stress; neuronal cells; mitochondria
- Citation
- Journal of Microbiology and Biotechnology, v.28, no.1, pp 40 - 49
- Pages
- 10
- Indexed
- SCIE
SCOPUS
KCI
- Journal Title
- Journal of Microbiology and Biotechnology
- Volume
- 28
- Number
- 1
- Start Page
- 40
- End Page
- 49
- URI
- https://scholarworks.gnu.ac.kr/handle/sw.gnu/12026
- DOI
- 10.4014/jmb.1710.10043
- ISSN
- 1017-7825
1738-8872
- Abstract
- We evaluated the antioxidant activity and neuronal cell-protective effect of fucoidan extract from Ecklonia cava (FEC) on hydrogen peroxide (H2O2)-induced cytotoxicity in PC-12 and MC-IXC 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 H2O2-treated PC-12 and MC-IXC cells. Based on the neuronal cell-protective effects, mitochondrial function was analyzed in PC-12 cells, and FEC significantly restored mitochondrial damage by increasing the mitochondrial membrane potential (Delta Psi m) 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 (IC50 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.
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