ArticleJournal of inflammation (London, England)2006
Effects of anti-inflammatory [1, 2, 4]triazolo[4, 3-a] [1, 8]naphthyridine derivatives on human stimulated PMN and endothelial cells: an in vitro study.
Article in Journal of inflammation (London, England), 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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Who cites it
3 citing papers in PubMed, 24 citations in OpenAlex.
- A Novel 1,8-Naphthyridine-2-Carboxamide Derivative Attenuates Inflammatory Responses and Cell Migration in LPS-Treated BV2 Cells via the Suppression of ROS Generation and TLR4/Myd88/NF-κB Signaling Pathway.International journal of molecular sciences · 2021Article
- General pathway for a convenient one-pot synthesis of trifluoromethyl-containing 2-amino-7-alkyl(aryl/heteroaryl)-1,8-naphthyridines and fused cycloalkane analogues.Molecules (Basel, Switzerland) · 2011Article
- Human neutrophil peptides upregulate expression of COX-2 and endothelin-1 by inducing oxidative stress.American journal of physiology. Heart and circulatory physiology · 2008Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background124 triazolo [4, 3-a]18naphthyridine derivatives (including NF161 and NF177) were tested for anti-inflammatory, analgesic and antipyretic properties and for their effects on spontaneous locomotor activity in mice and acute gastrolesivity in rats. Both NF161 and NF177 appeared to be anti-inflammatory and analgesic agents without toxic effects or acute gastrolesivity, but NF161 showed stronger anti-inflammatory activity, whereas NF177 was more active as analgesic.
methodsAn EIA kit was used to investigate the ability of NF161 and NF177 to affect prostaglandin E2 (PGE2) and prostacyclin (PGI2) production by human umbilical vascular endothelial cells (HUVEC). The compounds' effects on the production of reactive oxygen species (ROS) by human polymorphonuclear cells (PMNs) were studied in an in vitro cell model, evaluating inhibition of superoxide anion (O2-*) production induced by N-formylmethionyl-leucyl-phenylalanine (FMLP). Their effects on PMN adhesion to HUVEC were also investigated; they were incubated with PMNs and endothelial cells (EC) and challenged by stimuli including Platelet Activating Factor (PAF), FMLP, Phorbol Myristate Acetate (PMA), Tumor Necrosis Factor-alpha (TNF-alpha) and Interleukin-1beta (IL-1beta). Adhesion was quantitated by computerized micro-imaging fluorescence analysis.
resultsNeither compounds modified PGE2 or PGI2 production induced by IL-1alpha. O2-* production and myeloperoxidase release from PMNs stimulated by FMLP was inhibited in a dose- but not time-dependent manner by both 18naphthyridine derivatives, NF161 being statistically more active than NF177 (P < 0.01). The compounds inhibited adhesion evoked by the pro-inflammatory stimuli PAF, FMLP, TNF-alpha and IL-1beta in a concentration-dependent manner in the 10(-6)-10(-4)M range, being more active when PAF was used as stimulus and inactive when cells were challenged by PMA. Both compounds acted both on PMN and HUVEC.
conclusionConsidering the interesting anti-inflammatory effects of these compounds in in vivo models and the absence of acute gastrolesivity, the study improved knowledge of anti-inflammatory properties of NF161 and NF177, also demonstrating their potential in vitro, through inhibition of O2-* production, myeloperoxidase release and PMN adhesion to HUVEC. Negative results on PG production suggest a cyclooxygenase (COX)-independent mechanism.
Identifiers
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.