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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. 7.

Fig. 7.

TLR4 activation is associated with metabolic changes and inflammatory response in the liver but the phenotypic liver injury is predominantly absent. A. Quantitative real-time PCR (qRTPCR) analysis principle carbohydrate metabolic markers (PFK, GLUT-1, and GLUT-4) and fat metabolic markers (SREBP1c, PPAR-α, and PPAR-γ) in the liver tissue. mRNA expression of SREBP1c, PPAR-α, PPAR-γ and PFK, GLUT-1, GLUT-4 and B. mRNA expression analysis of inflammatory marker IL-1β, MCP-1, TNF-α, and Kupffer cell activation marker CD68 were analyzed in the liver sample 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). C. mRNA expression of SREBP1c, PPAR-γ were analyzed in the primary human hepatocytes cells treated with lipopolysaccharide (LPS) and Co-treated with LPS and sodium butyrate (LPS + NaBT). Normalized mRNA expression is represented as a fold change of Vehicle control (Veh Cont) on Y-axis. Data points represented with Mean ± SEM *(p < 0.05). D. Representative Hematoxylin and Eosin stained (H&E) images of liver sections showed liver pathophysiology of vehicle control group of mice (Veh, n = 3), gulf war chemical treated a group of mice (GWI, n = 3). Images were taken at 10× magnification.