ArticleChemico-biological interactions2016
Effects of a pyrrole-based, microtubule-depolymerizing compound on RAW 264.7 macrophages.
Article in Chemico-biological interactions, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 5 citations in OpenAlex.
- Physicochemical and Inflammatory Analysis of Unconjugated and Conjugated Bone-Binding Carbon Dots.ACS omega · 2024Article
- The In Vitro Proinflammatory Properties of Water Accommodated Sediment Extracts from a Creosote-Contaminated US Environmental Protection Agency Superfund Site.Environmental toxicology and chemistry · 2021Article
- Effects of a novel microtubule-depolymerizer on pro-inflammatory signaling in RAW264.7 macrophages.Chemico-biological interactions · 2018Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
RAW 264.7 murine macrophages were exposed to the pyrrole-based compound 3,5-Dibromo-4-(3,4-dimethoxyphenyl)-1H-pyrrole-2-carboxylic acid ethyl ester (JG-03-14), which is a known microtubule depolymerizing agent with antitumor activity [1,2,3]. In this study exposure to JG-03-14 reduced the production of pro-inflammatory molecules by macrophages activated with lipopolysaccharide (LPS). Treatment with the pyrrole-based compound decreased the concentration of tumor necrosis factor-α (TNF-α) and nitric oxide (NO) released from the macrophages. Exposure to JG-03-14 also decreased TNF-α mRNA expression levels and the protein expression levels of inducible nitric oxide synthase (iNOS), the enzyme responsible for NO production in the activated macrophages. Furthermore, JG-03-14 treatment significantly changed the degradation profile of IκB-β, an inhibitor of the NF-κB transcription factor, which suggests that JG-03-14 may attenuate the activation of the LPS-induced NF-κB signaling pathway needed to produce the pro-inflammatory mediators. We conclude that JG-03-14 possesses anti-inflammatory properties.
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Registered trials
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