Bibliographic Details
| Title: |
Anti-Inflammatory Effects of a Mytilus coruscus α-d-Glucan (MP-A) in Activated Macrophage Cells via TLR4/NF-κB/MAPK Pathway Inhibition |
| Authors: |
Fuyan Liu, Xiaofeng Zhang, Yuqiu Li, Qixin Chen, Fei Liu, Xiqiang Zhu, Li Mei, Xinlei Song, Xia Liu, Zhigang Song, Jinhua Zhang, Wen Zhang, Peixue Ling, Fengshan Wang |
| Source: |
Marine Drugs, Vol 15, Iss 9, p 294 (2017) |
| Publisher Information: |
MDPI AG, 2017. |
| Publication Year: |
2017 |
| Collection: |
LCC:Biology (General) |
| Subject Terms: |
THP-1 macrophages, anti-inflammatory, TLR4, NF-κB, MAPK, SPR analysis, Biology (General), QH301-705.5 |
| More Details: |
The hard-shelled mussel (Mytilus coruscus) has been used as Chinese traditional medicine for thousands of years; however, to date the ingredients responsible for the various beneficial health outcomes attributed to Mytilus coruscus are still unclear. An α-d-Glucan, called MP-A, was isolated from Mytilus coruscus, and observed to exert anti-inflammatory activity in THP-1 human macrophage cells. Specifically, we showed that MP-A treatment inhibited the production of inflammatory markers, including TNF-α, NO, and PGE2, inducible NOS (iNOS), and cyclooxygenase-2 (COX-2), in LPS-activated THP-1 cells. It was also shown to enhance phagocytosis in the analyzed cells, but to severely inhibit the phosphorylation of mitogen-activated protein kinases (MAPKs) and the nuclear translocation of NF-κB P65. Finally, MP-A was found to exhibit a high binding affinity for the cell surface receptor TLR4, but a low affinity for TLR2 and dectin-1, via surface plasmon resonance (SPR) analysis. The study indicates that MP-A suppresses LPS-induced TNF-α, NO and PEG2 production via TLR4/NF-κB/MAPK pathway inhibition, and suggests that MP-A may be a promising therapeutic candidate for diseases associated with TNF-α, NO, and/or PEG2 overproduction. |
| Document Type: |
article |
| File Description: |
electronic resource |
| Language: |
English |
| ISSN: |
1660-3397 |
| Relation: |
https://www.mdpi.com/1660-3397/15/9/294; https://doaj.org/toc/1660-3397 |
| DOI: |
10.3390/md15090294 |
| Access URL: |
https://doaj.org/article/811c98650da344d3b9771a699dbb689b |
| Accession Number: |
edsdoj.811c98650da344d3b9771a699dbb689b |
| Database: |
Directory of Open Access Journals |
