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. Author manuscript; available in PMC: 2019 Jul 1.
Published in final edited form as: Toxicol Appl Pharmacol. 2018 May 9;350:64–77. doi: 10.1016/j.taap.2018.05.006

Fig. 4.

Fig. 4.

Sodium butyrate priming in a rodent model of GWI improves proinflammatory phenotype in small intestine mediated by the TLR4 pathway. A. Small intestine tissue slices were probed for IL-1β immunoreactivity in vehicle control group of mice (Veh, n = 3), gulf war chemical treated group of mice (GWI, n = 3) and a group of mice co-exposed with GWI and sodium butyrate (GWI + NaBT, n = 3) using immunohistochemistry. Specific immunoreactivity to IL-1β is evident by dark brown spots. B. Graphical representation of morphometric analysis of the IL-1β immunoreactivity in tissue slices. Data normalized against vehicle control (veh) *(p < 0.05). C. Quantitative real-time PCR (qRTPCR) analysis of inflammatory markers in the small intestine. mRNA expression of IL-1β, MCP-1, and TNF-α was analyzed in the samples of vehicle control group of mice (Veh, n = 3), gulf war chemical treated group of mice (GWI, n = 3) and a group of mice co-exposed with GWI and sodium butyrate (GWI + NaBT, n = 3). Normalized mRNA expression is represented as a fold change of vehicle control (veh) on Y-axis. Data points represented with Mean ± SEM *(p < 0.05). D. Graphical representation of serum IL-1β in pg/mL of the samples of vehicle control group of mice (Veh, n = 3), gulf war chemical treated group of mice (GWI, n = 3) and a group of mice co-exposed with GWI and sodium butyrate (GWI + NaBT, n = 3). (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)