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Date of Award

2015

Document Type

Restricted Thesis: Campus only access

Degree Name

Bachelor of Science

Department

Biochemistry & Molecular Biol.

First Advisor

Dr. Krista Stenger

Abstract

Macrophages are key mediators of the inflammatory response. They are activated in the presence of conserved antigen molecules, triggering the NF-κB signaling cascade to promote pro-inflammatory and anti-pathogenic genes. RAW264.7 murine macrophages were subjected to treatment with 3,5-Dibromo-4-(3,4-dimethoxyphenyl)- 1H-pyrrole-2-carboxylic acid ethyl ester (JG-03-14), a known microtubule depolymerizing compound and antitumor agent.1,2 Treatment with JG-03-14 was found to alter the production levels of TNF-α, inducible nitric oxide synthase, and nitric oxide in macrophages activated with lipopolysaccharide. JG-03-14 also decreased the activated macrophages' TNF-α mRNA expression levels. Furthermore, JG-03-14 significantly changed the degradation profile of IκB-β after cells were activated with JG-03-14, which suggests that JG-03-14 attenuates the activation of the LPS-induced NF-κB signaling pathway contributing to the reduction in pro-inflammatory mediators. We conclude that JG-03-14 possesses anti-inflammatory properties.

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