ArticleBMB reports2018
Anti-inflammatory effects of a novel compound, MPQP, through the inhibition of IRAK1 signaling pathways in LPS-stimulated RAW 264.7 macrophages.
Article in BMB reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- Amino Derivatives of Diaryl Pyrimidines and Azolopyrimidines as Protective Agents against LPS-Induced Acute Lung Injury.Molecules (Basel, Switzerland) · 2023Article
- Synthesis, characterization, crystal structure and Hirshfeld surface analysis of a hexa-hydro-quinoline derivative:Acta crystallographica. Section E, Crystallographic communications · 2022Article
- Discovery of Nitro-azolo[1,5-Pharmaceuticals (Basel, Switzerland) · 2022Article
- lncRNA AK085865 Promotes Macrophage M2 Polarization in CVB3-Induced VM by Regulating ILF2-ILF3 Complex-Mediated miRNA-192 Biogenesis.Molecular therapy. Nucleic acids · 2020Article
- Anti-Inflammatory and Anti-Oxidative Effects of luteolin-7-International journal of molecular sciences · 2020Article
- An alpha-lipoic acid-decursinol hybrid compound attenuates lipopolysaccharide-mediated inflammation in BV2 and RAW264.7 cells.BMB reports · 2019Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Small-molecule inhibitors are widely used to treat a variety of inflammatory diseases. In this study, we found a novel antiinflammatory compound, 1-[(2R,4S)-2-methyl-4-(phenylamino)-1,2,3,4-tetrahydroquinolin-1-yl]prop-2-en-1-one (MPQP). It showed strong anti-inflammatory effects in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages. These effects were exerted through the inhibition of the production of NO and pro-inflammatory cytokines, such as interleukin (IL)-6, IL-1β, and tumor necrosis factor-α (TNF-α). Furthermore, MPQP decreased the expression levels of inducible NO synthase (iNOS) and cyclooxygenase 2 (COX-2). Additionally, it mediated the inhibition of the phosphorylation of p38, c-Jun N-terminal kinase (JNK), the inhibitor of κBα (IκBα), and their upstream kinases, IκB kinase (IKK) α/β, mitogen-activated protein kinase kinase (MKK) 3/6, and MKK4. Furthermore, the expression of IL-1 receptor-associated kinase 1 (IRAK1) that regulates NF-κB, p38, and the JNK signaling pathways, was also increased by MPQP. These results indicate that MPQP regulates the IRAK1-mediated inflammatory signaling pathways by targeting IRAK1 or its upstream factors. [BMB Reports 2018; 51(6): 308-313].
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