title: Honokiol inhibits LPS-induced maturation and inflammatory response of human monocyte-derived dendritic cells.
abstract: Honokiol (HNK) is a phenolic compound isolated from the bark of houpu (Magnolia officinalis), a plant widely used in traditional Chinese and Japanese medicine. While substantial evidence indicates that HNK possesses anti-inflammatory activity, its effect on dendritic cells (DCs) during the inflammatory reaction remains unclear. The present study investigates how HNK affects lipopolysaccharide (LPS)-stimulated human monocyte-derived DCs. Our experimental results show that HNK inhibits the inflammatory response of LPS-induced DCs by (1) suppressing the expression of CD11c, CD40, CD80, CD83, CD86, and MHC-II on LPS-activated DCs, (2) reducing the production of TNF-α, IL-1β, IL-6, and IL-12p70 but increasing the production of IL-10 and TGF-β1 by LPS-activated DCs, (3) inhibiting the LPS-induced DC-elicited allogeneic T-cell proliferation, and (4) shifting the LPS-induced DC-driven Th1 response toward a Th2 response. Further, our results show that HNK inhibits the phosphorylation levels of ERK1/2, p38, JNK1/2, IKKα, and IκBα in LPS-activated DCs. Collectively, the findings show that the anti-inflammatory actions of HNK on LPS-induced DCs are associated with the NF-κB and mitogen-activated protein kinase (MAPK) signaling pathways.
authors.affiliation: Department of Biomedical Engineering and Environmental Sciences, National Tsing Hua University, Hsinchu, Taiwan.
authors.forename: Chia-Yang
authors.initials: CY
authors.lastname: Li
authors.forename: Louis Kuoping
authors.initials: LK
authors.lastname: Chao
authors.forename: Shu-Chi
authors.initials: SC
authors.lastname: Wang
authors.forename: Hon-Zu
authors.initials: HZ
authors.lastname: Chang
authors.forename: Min-Lung
authors.initials: ML
authors.lastname: Tsai
authors.forename: Shih-Hua
authors.initials: SH
authors.lastname: Fang
authors.forename: Pei-Chun
authors.initials: PC
authors.lastname: Liao
authors.forename: Chen-Lung
authors.initials: CL
authors.lastname: Ho
authors.forename: Shui-Tein
authors.initials: ST
authors.lastname: Chen
authors.forename: Wei-Chung
authors.initials: WC
authors.lastname: Cheng
authors.forename: Chi-Shiun
authors.initials: CS
authors.lastname: Chiang
authors.forename: Yueh-Hsiung
authors.initials: YH
authors.lastname: Kuo
authors.forename: Kuo-Feng
authors.initials: KF
authors.lastname: Hua
authors.forename: Ian C
authors.initials: IC
authors.lastname: Hsu
mesh_terms: D001713:Biphenyl Compounds / Q000494:pharmacology*; D002454:Cell Differentiation / Q000187:drug effects*; D002460:Cell Line; D049109:Cell Proliferation / Q000187:drug effects; D002470:Cell Survival / Q000187:drug effects; D016207:Cytokines / Q000096:biosynthesis; D003713:Dendritic Cells / Q000166:cytology* / Q000187:drug effects / Q000201:enzymology / Q000276:immunology*; D004705:Endocytosis / Q000187:drug effects; D004789:Enzyme Activation / Q000187:drug effects; D006801:Humans; D007249:Inflammation / Q000473:pathology*; D017705:Lignans / Q000494:pharmacology*; D008070:Lipopolysaccharides / Q000494:pharmacology*; D020935:MAP Kinase Signaling System / Q000187:drug effects; D020928:Mitogen-Activated Protein Kinases / Q000378:metabolism; D009000:Monocytes / Q000166:cytology*; D016328:NF-kappa B / Q000378:metabolism; D010641:Phenotype; D018417:Th1 Cells / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D018418:Th2 Cells / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D000498:Allyl Compounds; D010636:Phenols
chemical_list: D001713:Biphenyl Compounds; D016207:Cytokines; D017705:Lignans; D008070:Lipopolysaccharides; D020928:Mitogen-Activated Protein Kinases; D016328:NF-kappa B; C005499:honokiol; D000498:Allyl Compounds; D010636:Phenols