Fig. 5: IPA inhibits the activation of NF-κB signaling and the production of proinflammatory cytokines in macrophages in response to endotoxin. | Experimental & Molecular Medicine

Fig. 5: IPA inhibits the activation of NF-κB signaling and the production of proinflammatory cytokines in macrophages in response to endotoxin.

From: Indole-3-propionic acid inhibits gut dysbiosis and endotoxin leakage to attenuate steatohepatitis in rats

Fig. 5

a, b IPA inhibits NF-kB signaling in murine J774A.1 macrophages. Cells were pretreated with IPA (250 μM and 500 μM) for 1 h, followed by 500 ng/mL LPS treatment for an additional 30 min. a Representative immunoblots are shown. b Expression levels of proinflammatory cytokines were determined by real-time PCR. Relative expression levels were normalized to those of GAPDH. The data are presented as the mean ± SEM (n = 4). *P < 0.05 vs. vehicle; #P < 0.05 vs. LPS treatment. c–f IPA inhibits NF-κB signaling in the livers of HFD-fed rats. Representative immunoblots (c) and densitometric quantification (d) from three rats in each group are shown. Relative phosphorylation levels were normalized to those of endogenous proteins except for phosphorylated IκBα, which was normalized to β-actin. The expression levels of cytokine genes (TNFα, IL-1β, and IL-6) (e) and chemokine genes (CCL2 and CCR2) (f) were determined by real-time PCR. Relative expression levels were normalized to those of GAPDH. The data are presented as the mean ± SEM. n = 7–10, *P < 0.05, vs. rats fed a chow diet; #P < 0.05, vs. rats fed a high-fat diet

Back to article page