Biomol Ther (Seoul)  
Protective Role of Fucoidan in Cerebral Ischemia-Reperfusion Injury through Inhibition of MAPK Signaling Pathway
Nan Che1, Yijie Ma2 and Yinhu Xin3,*
1Department of Neurology, Ninth Hospital of Xi’an, Xi’an 710054, Shaanxi,
2Department of Neurological Surgery, Hospital of Xinjiang Production and Construction Corps, Urumchi 830002, Xinjiang,
3Department of Encephalopathy, Shaanxi Traditional Chinese Medicine Hospital, Xi’an 710003, Shaanxi, China
E-mail: xinyinhu6887@126.com
Tel: +86-17186416584, Fax: +86-17186416584
Received: May 9, 2016; Revised: August 2, 2016; Accepted: September 1, 2016; Published online: November 25, 2016.
© The Korean Society of Applied Pharmacology. All rights reserved.

Abstract
Fucoidan has been reported to exhibit various beneficial activities ranging from to antivirus and anticancer properties. However, little information is available about the effects of fucoidan on cerebral ischemia-reperfusion injury (IRI). Our study aimed to explore the effects of fucoidan on cerebral IRI, as well as the underlying mechanisms. Sprague-Dawley (SD) rats were randomly subjected to four groups: Sham, IRI+saline (IRI+S), IRI+80 mg/kg fucoidan (IRI+F80), and IRI+160 mg/kg fucoidan (IRI+F160). Fucoidan (80 mg/kg or 160 mg/kg) was intraperitoneally injected from 7 days before the rats were induced to cerebral IRI model with middle cerebral artery occlusion (MCAO) method. At 24 h after reperfusion, neurological deficits and the total infarct volume were determined. The levels of inflammation-associated cytokines (interleukin (IL)-1β, IL-6, myeloperoxidase (MPO), and tumor necrosis factor (TNF)-α), oxidative stress-related proteins (malondialdehyde (MDA) and superoxide dismutase (SOD)) in the ischemic brain were measured by enzyme-linked immunosorbent assay (ELISA). Besides, the levels of apoptosis-related proteins (p-53, Bax, and B-cell lymphoma (Bcl)-2) and mitogen-activated protein kinase (MAPK) pathway (phosphorylation-extracellular signalregulated kinase (p-ERK), p-c-Jun N-terminal kinase (JNK), and p-p38) were measured. Results showed that administration of fucoidan significantly reduced the neurological deficits and infarct volume compared to the IRI+S group in a dose-dependent manner. Also, fucoidan statistically decreased the levels of inflammation-associated cytokines, and oxidative stress-related proteins, inhibited apoptosis, and suppressed the MAPK pathway. So, Fucoidan plays a protective role in cerebral IRI might be by inhibition of MAPK pathway.
Keywords: Fucoidan, Cerebral ischemia-reperfusion injury, MAPK pathway


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