共 53 条
Ishige okamurae Attenuates Neuroinflammation and Cognitive Deficits in Mice Intracerebroventricularly Injected with LPS via Regulating TLR-4/MyD88-Dependent Pathways
被引:9
作者:

Kwon, Oh-Yun
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机构:
Incheon Natl Univ, Dept Nano bioengn, Acad ro 119, Incheon 22012, South Korea Incheon Natl Univ, Dept Nano bioengn, Acad ro 119, Incheon 22012, South Korea

Lee, Seung-Ho
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Incheon Natl Univ, Dept Nano bioengn, Acad ro 119, Incheon 22012, South Korea Incheon Natl Univ, Dept Nano bioengn, Acad ro 119, Incheon 22012, South Korea
机构:
[1] Incheon Natl Univ, Dept Nano bioengn, Acad ro 119, Incheon 22012, South Korea
关键词:
Ishige okamurae;
lipopolysaccharide;
neuroinflammation;
cognitive deficits;
TLR-4;
MyD88;
CELL ACTIVATION;
INFLAMMATION;
IMPAIRMENT;
D O I:
10.3390/antiox12010078
中图分类号:
Q5 [生物化学];
Q7 [分子生物学];
学科分类号:
071010 ;
081704 ;
摘要:
Neuroinflammation is one of the critical causes of neuronal loss and cognitive impairment. We aimed to evaluate the anti-neuroinflammatory properties of Ishige okamuae using mice intracerebroventricularly injected with lipopolysaccharides (LPS) and LPS-treated C6 glioma cells. We found that the short- and long-term memory deficits of LPS-injected mice were improved by oral administration of Ishige okamurae extracts (IOE). LPS-induced neuronal loss, increase in amyloid-beta plaque, and expression of COX-2 and iNOS were restored by IOE. In addition, LPS-induced activation of Toll-like receptor-4 (TLR-4) and its downstream molecules, such as MyD88, NF kappa B, and mitogen-activated protein kinases (MAPKs), were significantly attenuated in the brains of mice fed with IOE. We found that pretreatment of IOE to C6 glioma cells ameliorated LPS-induced expression of TLR-4 and its inflammatory cascades, such as MyD88 expression, reactive oxygen species production, MAPKs phosphorylation, and NF kappa B phosphorylation with consequent downregulation of COX-2, iNOS, proinflammatory cytokines, and nitric oxide expression. Furthermore, IOE (0.2 mu g/mL) was found to have equivalent efficacy with 10 mu M of MyD88 inhibitor in preventing LPS-induced inflammatory responses in C6 glioma cells. Taken together, these results strongly suggest that IOE could be developed as a promising anti-neuroinflammatory agent which is able to control the TLR-4/MyD88-dependent signaling pathways.
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