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dc.contributor.authorLi, Xiaoling
dc.contributor.authorHuang, Riming
dc.contributor.authorLiu, Kaifeng
dc.contributor.authorLi, Mingyue
dc.contributor.authorLuo, Hui
dc.contributor.authorCui, Liao
dc.contributor.authorHuang, Lei
dc.contributor.authorLuo, Lianxiang
dc.date2022-08-11T08:09:58.000
dc.date.accessioned2022-08-23T16:50:38Z
dc.date.available2022-08-23T16:50:38Z
dc.date.issued2020-12-11
dc.date.submitted2021-01-28
dc.identifier.citation<p>Li X, Huang R, Liu K, Li M, Luo H, Cui L, Huang L, Luo L. Fucoxanthin attenuates LPS-induced acute lung injury via inhibition of the TLR4/MYD88 signaling axis. Aging (Albany NY). 2020 Dec 11;13(2):2655-2667. doi: 10.18632/aging.202309. Epub ahead of print. PMID: 33323555. <a href="https://doi.org/10.18632/aging.202309">Link to article on publisher's site</a></p>
dc.identifier.issn1945-4589 (Linking)
dc.identifier.doi10.18632/aging.202309
dc.identifier.pmid33323555
dc.identifier.urihttp://hdl.handle.net/20.500.14038/41696
dc.description.abstractAcute lung injury (ALI) is a critical clinical condition with a high mortality rate. It is believed that the inflammatory storm is a critical contributor to the occurrence of ALI. Fucoxanthin is a natural extract from marine seaweed with remarkable biological properties, including antioxidant, anti-tumor, and anti-obesity. However, the anti-inflammatory activity of Fucoxanthin has not been extensively studied. The current study aimed to elucidate the effects and the molecular mechanism of Fucoxanthin on lipopolysaccharide-induced acute lung injury. In this study, Fucoxanthin efficiently reduced the mRNA expression of pro-inflammatory factors, including IL-10, IL-6, iNOS, and Cox-2, and down-regulated the NF-kappaB signaling pathway in Raw264.7 macrophages. Furthermore, based on the network pharmacological analysis, our results showed that anti-inflammation signaling pathways were screened as fundamental action mechanisms of Fucoxanthin on ALI. Fucoxanthin also significantly ameliorated the inflammatory responses in LPS-induced ALI mice. Interestingly, our results revealed that Fucoxanthin prevented the expression of TLR4/MyD88 in Raw264.7 macrophages. We further validated Fucoxanthin binds to the TLR4 pocket using molecular docking simulations. Altogether, these results suggest that Fucoxanthin suppresses the TLR4/MyD88 signaling axis by targeting TLR4, which inhibits LPS-induced ALI, and fucoxanthin inhibition may provide a novel strategy for controlling the initiation and progression of ALI.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=33323555&dopt=Abstract">Link to Article in PubMed</a></p>
dc.rightsCopyright: © 2020 Li et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
dc.rights.urihttp://creativecommons.org/licenses/by/3.0/
dc.subjectacute lung injury
dc.subjectfucoxanthin
dc.subjectLPS
dc.subjectTLR4
dc.subjectMyD88
dc.subjectNF-κB
dc.subjectCell Biology
dc.subjectCellular and Molecular Physiology
dc.subjectMolecular Biology
dc.subjectRespiratory Tract Diseases
dc.titleFucoxanthin attenuates LPS-induced acute lung injury via inhibition of the TLR4/MYD88 signaling axis
dc.typeJournal Article
dc.source.journaltitleAging
dc.source.volume13
dc.source.issue2
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=5515&amp;context=oapubs&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/4485
dc.identifier.contextkey21308485
refterms.dateFOA2022-08-23T16:50:38Z
html.description.abstract<p>Acute lung injury (ALI) is a critical clinical condition with a high mortality rate. It is believed that the inflammatory storm is a critical contributor to the occurrence of ALI. Fucoxanthin is a natural extract from marine seaweed with remarkable biological properties, including antioxidant, anti-tumor, and anti-obesity. However, the anti-inflammatory activity of Fucoxanthin has not been extensively studied. The current study aimed to elucidate the effects and the molecular mechanism of Fucoxanthin on lipopolysaccharide-induced acute lung injury. In this study, Fucoxanthin efficiently reduced the mRNA expression of pro-inflammatory factors, including IL-10, IL-6, iNOS, and Cox-2, and down-regulated the NF-kappaB signaling pathway in Raw264.7 macrophages. Furthermore, based on the network pharmacological analysis, our results showed that anti-inflammation signaling pathways were screened as fundamental action mechanisms of Fucoxanthin on ALI. Fucoxanthin also significantly ameliorated the inflammatory responses in LPS-induced ALI mice. Interestingly, our results revealed that Fucoxanthin prevented the expression of TLR4/MyD88 in Raw264.7 macrophages. We further validated Fucoxanthin binds to the TLR4 pocket using molecular docking simulations. Altogether, these results suggest that Fucoxanthin suppresses the TLR4/MyD88 signaling axis by targeting TLR4, which inhibits LPS-induced ALI, and fucoxanthin inhibition may provide a novel strategy for controlling the initiation and progression of ALI.</p>
dc.identifier.submissionpathoapubs/4485
dc.contributor.departmentDepartment of Molecular, Cell and Cancer Biology
dc.source.pages2655-2667


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Copyright: © 2020 Li et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Except where otherwise noted, this item's license is described as Copyright: © 2020 Li et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.