SM905, an artemisinin derivative, inhibited NO and pro-inflammatory cytokine production by suppressing MAPK and NF-κB pathways in RAW 264.7 macrophages
文献类型：期刊论文
| 作者 | Junxia WANG5; Lifei HOU4; Yang YANG3; Wei TANG2 ; Ying LI1; Jianping ZUO3
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| 刊名 | Acta Pharmacologica Sinica
 |
| 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/2S10ELR8/293935]  |
| 专题 | 中国科学院上海药物研究所 |
| 作者单位 | 1.Department of Synthetic Chemistry,Shanghai Institute of Materia Medica,Chinese Academy of Sciences 2.中国科学院上海药物研究所 3.Laboratory of Immunology and Virology,Shanghai Uni-versity of Traditional Chinese Medicine 4.Laboratory of Immunopharmacology, Shanghai Institute of Materia Medic 5.中国科学院上海生命科学研究院 |
| 推荐引用方式 GB/T 7714 | Junxia WANG,Lifei HOU,Yang YANG,et al. SM905, an artemisinin derivative, inhibited NO and pro-inflammatory cytokine production by suppressing MAPK and NF-κB pathways in RAW 264.7 macrophages[J]. Acta Pharmacologica Sinica,2009,30(10):1428. |
| APA | Junxia WANG,Lifei HOU,Yang YANG,Wei TANG,Ying LI,&Jianping ZUO.(2009).SM905, an artemisinin derivative, inhibited NO and pro-inflammatory cytokine production by suppressing MAPK and NF-κB pathways in RAW 264.7 macrophages.Acta Pharmacologica Sinica,30(10),1428. |
| MLA | Junxia WANG,et al."SM905, an artemisinin derivative, inhibited NO and pro-inflammatory cytokine production by suppressing MAPK and NF-κB pathways in RAW 264.7 macrophages".Acta Pharmacologica Sinica 30.10(2009):1428. |
入库方式： OAI收割
来源：上海药物研究所
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