title: Naringin inhibits chemokine production in an LPS-induced RAW 264.7 macrophage cell line.
abstract: Naringin has been reported to act as an effective anti-inflammatory compound.             In a previous study, we demonstrated that the anti-inflammatory effect of naringin             on lipopolysaccharide (LPS)-induced acute lung injury in mice correlated with             the inhibition of the nuclear factor-κB (NF-κB) pathway. However, the effects             and mechanism of action of naringin on LPS-induced chemokine expression are not             yet fully understood. This study aimed to evaluate the effect of naringin on chemokine             expression in LPS-induced RAW 264.7 macrophages and to provide insights into the             possible underlying mechanisms. We found that the in vitro pre-treatment with             naringin led to a significant attenuation in the LPS-induced secretion of interleukin-8             (IL-8), monocyte chemoattractant protein-1 (MCP-1) and macrophage inflammatory             protein-1α (MIP-1α). RT-qPCR demonstrated that naringin significantly reduced             the LPS-induced upregulation of IL-8, MCP-1 and MIP-1α mRNA expression in a dose-dependent             manner. Additionally, western blot analysis revealed that naringin effectively             suppressed NF-κB activation by inhibiting the degradation of IκB-α and the translocation             of p65. Naringin also attenuated MAPK activation by inhibiting the phosphorylation             of ERK1/2, JNK and p38 MAPK. Taken together, these demonstrate that naringin reduces             IL-8, MCP-1 and MIP-1α secretion and mRNA expression, possibly by blocking the             activation of the NF-κB and MAPK signaling pathways in LPS-induced RAW 264.7 macrophages.
authors.affiliation: Key Laboratory of Gene Engineering of the Ministry of Education and Guangdong Key Laboratory of Plant Resources, School of Life Sciences, Sun Yat-sen University, Guangzhou, Guangdong 510275, P.R. China.
authors.forename: Ying
authors.initials: Y
authors.lastname: Liu
authors.forename: Wei-wei
authors.initials: WW
authors.lastname: Su
authors.forename: Sheng
authors.initials: S
authors.lastname: Wang
authors.forename: Pei-bo
authors.initials: PB
authors.lastname: Li
mesh_terms: D000818:Animals; D002460:Cell Line; D054405:Chemokine CCL3 / Q000235:genetics / Q000378:metabolism; D018925:Chemokines / Q000235:genetics / Q000378:metabolism*; D044950:Flavanones / Q000494:pharmacology*; D015870:Gene Expression / Q000187:drug effects*; D020672:I-kappa B Proteins / Q000378:metabolism; D016209:Interleukin-8 / Q000235:genetics / Q000378:metabolism; D048031:JNK Mitogen-Activated Protein Kinases / Q000378:metabolism; D008070:Lipopolysaccharides / Q000633:toxicity; D008264:Macrophages / Q000187:drug effects; D051379:Mice; D019950:Mitogen-Activated Protein Kinase 1 / Q000378:metabolism; D048052:Mitogen-Activated Protein Kinase 3 / Q000378:metabolism; D000072000:NF-KappaB Inhibitor alpha; D016328:NF-kappa B / Q000378:metabolism; D010766:Phosphorylation / Q000187:drug effects; D012333:RNA, Messenger / Q000378:metabolism; D054390:Receptors, CCR2 / Q000235:genetics / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects; D051996:Transcription Factor RelA / Q000378:metabolism; D048051:p38 Mitogen-Activated Protein Kinases / Q000378:metabolism
chemical_list: D054405:Chemokine CCL3; D018925:Chemokines; D044950:Flavanones; D020672:I-kappa B Proteins; D016209:Interleukin-8; D008070:Lipopolysaccharides; D016328:NF-kappa B; C000606205:Nfkbia protein, mouse; D012333:RNA, Messenger; D054390:Receptors, CCR2; D051996:Transcription Factor RelA; D000072000:NF-KappaB Inhibitor alpha; D048031:JNK Mitogen-Activated Protein Kinases; D019950:Mitogen-Activated Protein Kinase 1; D048052:Mitogen-Activated Protein Kinase 3; D048051:p38 Mitogen-Activated Protein Kinases; C005274:naringin