中国科学院机构知识库网格
Chinese Academy of Sciences Institutional Repositories Grid
sm905anartemisininderivativeinhibitednoandproinflammatorycytokineproductionbysuppressingmapkandnfbpathwaysinraw2647macrophages

文献类型:期刊论文

作者Junxia WANG1; Lifei HOU2; Yang YANG3; Wei TANG4; Ying LI5; Jianping ZUO3
刊名actapharmacologicasinica
出版日期2009
卷号30期号:10页码:1428
关键词artemisinin SM905 NO iNOS inflammation MAPK NF-κB cyclooxygenase 2 TLR4 receptor
ISSN号1671-4083
英文摘要Aim:To elucidate the anti-inflammatory potentials and underlying mechanisms of SM905, a novel artemisinin derivative, in lipopoly-saccharide (LPS)-stimulated murine macrophage RAW 264.7 cells.Methods: Nitric oxide (NO) generation, cytokine production, and the protein expression levels of inducible nitric-oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) were examined using a Griess assay, an enzyme-linked immunosorbent assay (ELISA) and a Western blotting assay, respectively. The mRNA expression was measured using real-time PCR. The phosphorylation of extracellular signal-regulated kinase1/2 (ERK1/2), p38, c-jun N-terminal kinase (JNK), and the degradation of IκBα were assessed by Western blotting analysis. The nuclear translocation of nuclear factor-κB (NF-κB) was observed using confocal microscopy.Results: Pretreatment with SM905 (0, 0.1, 1, and 10 μmol/L) suppressed LPS-induced NO, TNF-α, IL-1β, and IL-6 production, and decreased both protein and mRNA levels of iNOS and COX-2. The mRNA expression of LPS receptor Toll-like receptor 4 (TLR4) and myeloid differentiation protein-2 (MD-2) was not changed, while LPS-induced CD14 expression was slightly reduced after SM905 treat-ment. SM905 markedly decreased the activation of ERK1/2, p38 and JNK suppressed the degradation of IκBα, but did not modify the expression of interferon regulatory factor-1 (IRF-1), signal transducer and activator of transcription 1 (STAT1) or interferon-inducible pro-tein-10 (IP-10). By using confocal microscopy, we further observed that NF-κB was correspondingly inhibited in SMgO5-treated cells.Conclusion: SM905 inhibited NO and pro-inflammatory cytokine production in LPS-stimulated RAW 264.7 cells and these effects are at least partially mediated through suppression of the MAPK and NF-κB signaling pathways.
语种英语
源URL[http://119.78.100.183/handle/2S10ELR8/288124]  
专题中国科学院上海药物研究所
作者单位1.中国科学院上海生命科学研究院
2.Laboratory of Immunopharmacology, Shanghai Institute of Materia Medic
3.Laboratory of Immunology and Virology,Shanghai Uni-versity of Traditional Chinese Medicine
4.中国科学院上海药物研究所
5.Department of Synthetic Chemistry,Shanghai Institute of Materia Medica,Chinese Academy of Sciences
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GB/T 7714
Junxia WANG,Lifei HOU,Yang YANG,et al. sm905anartemisininderivativeinhibitednoandproinflammatorycytokineproductionbysuppressingmapkandnfbpathwaysinraw2647macrophages[J]. actapharmacologicasinica,2009,30(10):1428.
APA Junxia WANG,Lifei HOU,Yang YANG,Wei TANG,Ying LI,&Jianping ZUO.(2009).sm905anartemisininderivativeinhibitednoandproinflammatorycytokineproductionbysuppressingmapkandnfbpathwaysinraw2647macrophages.actapharmacologicasinica,30(10),1428.
MLA Junxia WANG,et al."sm905anartemisininderivativeinhibitednoandproinflammatorycytokineproductionbysuppressingmapkandnfbpathwaysinraw2647macrophages".actapharmacologicasinica 30.10(2009):1428.

入库方式: OAI收割

来源:上海药物研究所

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