Please use this identifier to cite or link to this item: https://doi.org/10.1186/s12906-017-1635-1
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dc.titleVaccaria hypaphorine alleviates lipopolysaccharide-induced inflammation via inactivation of NF?B and ERK pathways in Raw 264.7 cells
dc.contributor.authorSun, H
dc.contributor.authorCai, W
dc.contributor.authorWang, X
dc.contributor.authorLiu, Y
dc.contributor.authorHou, B
dc.contributor.authorZhu, X
dc.contributor.authorQiu, L
dc.date.accessioned2020-10-27T10:30:06Z
dc.date.available2020-10-27T10:30:06Z
dc.date.issued2017
dc.identifier.citationSun, H, Cai, W, Wang, X, Liu, Y, Hou, B, Zhu, X, Qiu, L (2017). Vaccaria hypaphorine alleviates lipopolysaccharide-induced inflammation via inactivation of NF?B and ERK pathways in Raw 264.7 cells. BMC Complementary and Alternative Medicine 17 (1) : 120. ScholarBank@NUS Repository. https://doi.org/10.1186/s12906-017-1635-1
dc.identifier.issn14726882
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/181298
dc.description.abstractBackground: Activation of macrophage is involved in many inflammation diseases. Lipopolysaccharide (LPS) is a powerful inflammatory signal contributing to monocytes/macrophages activation associated with increased proinflammatory cytokines expressions. We recently identified that vaccarin was expected to protect endothelial cells from injury. Hypaphorine was abundantly found in vaccaria semen. However, the potential roles and underlying mechanisms of vaccaria hypaphorine on macrophage inflammation have been poorly defined. Methods: This study was designed to determine the effects of vaccaria hypaphorine on LPS-mediated inflammation in RAW 264.7 cells. Results: In this study, we demonstrated that vaccaria hypaphorine dramatically ameliorated LPS-induced nitric oxide (NO) release and productions of proinflammatory cytokines including tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), IL-6, IL-10, monocyte chemoattractant protein 1 (MCP-1) and prostaglandin E2 (PGE2) in RAW 264.7 cells. LPS-stimulated expressions of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) were down-regulated by vaccaria hypaphorine. Furthermore, vaccaria hypaphorine retarded LPS-induced phosphorylation of ERK, nuclear factor kappa beta (NFΚB), NFΚB inhibitor IΚBα, and IKKβ. Immunofluorescence staining revealed that vaccaria hypaphorine eliminated the nuclear translocation of NFΚB in LPS-treated RAW 264.7 cells. Conclusion: It was seen that vaccaria hypaphorine counteracted inflammation via inhibition of ERK or/and NFΚB signaling pathways. Collectively, we concluded that vaccaria hypaphorine can be served as an anti-inflammatory candidate. © 2017 The Author(s).
dc.rightsAttribution 4.0 International
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.sourceUnpaywall 20201031
dc.subjectacetylsalicylic acid
dc.subjectantiinflammatory agent
dc.subjectcyclooxygenase 2
dc.subjectdexamethasone
dc.subjectherbaceous agent
dc.subjectI kappa B kinase alpha
dc.subjectI kappa B kinase beta
dc.subjectimmunoglobulin enhancer binding protein
dc.subjectinducible nitric oxide synthase
dc.subjectinterleukin 10
dc.subjectinterleukin 1beta
dc.subjectinterleukin 6
dc.subjectlipopolysaccharide
dc.subjectmessenger RNA
dc.subjectmitogen activated protein kinase
dc.subjectmonocyte chemotactic protein 1
dc.subjectnitric oxide
dc.subjectprostaglandin E2
dc.subjecttranscription factor RelA
dc.subjecttumor necrosis factor
dc.subjectunclassified drug
dc.subjectVaccaria hypaphorine
dc.subjectantiinflammatory agent
dc.subjectautacoid
dc.subjectcytokine
dc.subjectI kappa B kinase
dc.subjectI kappa B kinase alpha
dc.subjectimmunoglobulin enhancer binding protein
dc.subjectindole derivative
dc.subjectlenticin
dc.subjectnitric oxide
dc.subjectplant extract
dc.subjectanimal cell
dc.subjectantiinflammatory activity
dc.subjectArticle
dc.subjectcell viability
dc.subjectcellular distribution
dc.subjectconcentration response
dc.subjectcontrolled study
dc.subjectcytokine production
dc.subjectdown regulation
dc.subjectdrug effect
dc.subjectdrug mechanism
dc.subjectenzyme inhibition
dc.subjectenzyme phosphorylation
dc.subjectgene expression regulation
dc.subjecthuman
dc.subjecthuman cell
dc.subjectimmunofluorescence
dc.subjectin vitro study
dc.subjectinflammation
dc.subjectintracellular signaling
dc.subjectlipopolysaccharide induced inflammation
dc.subjectMCF-7 cell line
dc.subjectmolecular dynamics
dc.subjectmouse
dc.subjectnonhuman
dc.subjectoutcome assessment
dc.subjectRAW 264.7 cell line
dc.subjectanimal
dc.subjectchemically induced
dc.subjectchemistry
dc.subjectdrug effects
dc.subjectinflammation
dc.subjectmacrophage
dc.subjectmetabolism
dc.subjectphosphorylation
dc.subjectphytotherapy
dc.subjectRAW 264.7 cell line
dc.subjectsignal transduction
dc.subjecttransport at the cellular level
dc.subjectVaccaria
dc.subjectAnimals
dc.subjectAnti-Inflammatory Agents
dc.subjectBiological Transport
dc.subjectCyclooxygenase 2
dc.subjectCytokines
dc.subjectHumans
dc.subjectI-kappa B Kinase
dc.subjectIndoles
dc.subjectInflammation
dc.subjectInflammation Mediators
dc.subjectLipopolysaccharides
dc.subjectMacrophages
dc.subjectMAP Kinase Signaling System
dc.subjectMCF-7 Cells
dc.subjectMice
dc.subjectNF-kappa B
dc.subjectNF-KappaB Inhibitor alpha
dc.subjectNitric Oxide
dc.subjectNitric Oxide Synthase Type II
dc.subjectPhosphorylation
dc.subjectPhytotherapy
dc.subjectPlant Extracts
dc.subjectRAW 264.7 Cells
dc.subjectVaccaria
dc.typeArticle
dc.contributor.departmentDEPT OF PHARMACOLOGY
dc.description.doi10.1186/s12906-017-1635-1
dc.description.sourcetitleBMC Complementary and Alternative Medicine
dc.description.volume17
dc.description.issue1
dc.description.page120
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