Protective Role of Fucoidan in Cerebral Ischemia-Reperfusion Injury through Inhibition of MAPK Signaling Pathway.
10.4062/biomolther.2016.098
- Author:
Nan CHE
1
;
Yijie MA
;
Yinhu XIN
Author Information
1. Department of Neurology, Ninth Hospital of Xi'an, Xi'an 710054, Shaanxi, China.
- Publication Type:Original Article
- Keywords:
Fucoidan;
Cerebral ischemia-reperfusion injury;
MAPK pathway
- MeSH:
Animals;
Apoptosis;
Brain;
Cytokines;
Enzyme-Linked Immunosorbent Assay;
Infarction, Middle Cerebral Artery;
Interleukin-6;
Lymphoma, B-Cell;
Methods;
Peroxidase;
Phosphotransferases;
Protein Kinases;
Rats;
Rats, Sprague-Dawley;
Reperfusion;
Reperfusion Injury*;
Superoxide Dismutase;
Tumor Necrosis Factor-alpha
- From:Biomolecules & Therapeutics
2017;25(3):272-278
- CountryRepublic of Korea
- Language:English
-
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 signal-regulated 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.
