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.

Document Type

Post-print Article

Publication Date


Publisher Statement

Copyright © 2016 Elsevier Ireland Ltd.. Article first published online: JAN 2016.

DOI: 10.1016/j.cbi.2016.01.009

The definitive version is available at:

Full citation:

John A. Ciemniecki, Clarke P. Lewis, John T. Gupton, and Krista Fischer-Stenger. "Effects of a Pyrrole-Based, Microtubule-Depolymerizing Compound on RAW 264.7 Macrophages." In Chemico-Biological Interactions 246 (2016), 63-68. doi:10.1016/j.cbi.2016.01.009.