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. Author manuscript; available in PMC: 2015 Oct 1.
Published in final edited form as: J Hepatol. 2014 May 22;61(4):903–911. doi: 10.1016/j.jhep.2014.05.024

Figure 3. 17-DMAG treatment inhibits oxidative stress and decreases pro-inflammatory cytokine production.

Figure 3

Figure 3

Figure 3

Serum endotoxin (A), liver cytokine mRNA (B) and LM TNFα mRNA (C) analyzed by real time PCR. TNFα mRNA (D:left panel) and protein (D:right panel) was analyzed. LMs were pooled from 8 alcoholic mice stimulated ex-vivo with LPS ± 17-DMAG and percent down-regulation is depicted on each graph. CD14 and TLR4 mRNA (E) analyzed in 17-DMAG treated alcoholic liver. NFκB DNA binding activity (F) analyzed in LPS ± 17-DMAG treated alcoholic RAW macrophages [unlabeled competitor oligonucleotide (Comp)]. RAW macrophages transiently transfected with hsp90α siRNA or scrambled siRNA for 48hrs and knockdown confirmed in cellular lysates (G: upper panel) and supernatants analyzed for TNFα protein (G: lower panel). Hsp90 protein expression normalized to untransfected sample in respective group. Fold change in inflammatory subset cell markers in liver is shown (H). Bars represent mean ± SE, (n=6 mice; n=3 in vitro). **p<0.05, *p<0.0005, #p<0.00005, ns - not significant.