Skip to main content
Fig. 6 | Nutrition & Metabolism

Fig. 6

From: Dihydromyricetin ameliorates liver fibrosis via inhibition of hepatic stellate cells by inducing autophagy and natural killer cell-mediated killing effect

Fig. 6

DHM treatment induced IFN-γ production in NK cells through AhR-NF-κB/STAT3 signaling pathway. a, b NK92 cells were pretreated with DHM (10 μM) for 2 h and were exposed to TGF-β1 (5 ng/ml) for 24 h. The mRNA levels of (AhR) (a) and (CYP1A1) (b) were quantified by qRT-PCR assay. (C) NK92 cells were preincubated with CH223191 (10 μM) for 1 h to inhibit AhR. Thereafter, cells were treated with DHM (10 μM) for 2 h, then exposed to TGF-β1 (5 ng/ml) for another 24 h. The expressions of P-STAT3, STAT3, P-NF-κB and NF-κB were measured by western blot. d, e The bar graphs show the quantification of the indicated proteins. f, g Cells were treated as described in c. The mRNA level of IFN-γ was detected by qRT-PCR (f) and the expression level of IFN-γ in the medium was detected via ELISA (g). h, i STAT3 and NF-κB were knocked down by the corresponding inhibitor. After that, the cells were pretreated with DHM (10 μM) for 2 h and then incubated with TGF-β1 (5 ng/ml) for an additional 24 h. The bar charts show the mRNA level of IFN-γ by qRT-PCR (H) and the level of IFN-γ by ELISA assay (I). Data were presented as mean ± SEM (n = 3); **p < 0.01, compared to the control group; ##p < 0.01, compared to TGF-β1 group; $p < 0.05, $ $p < 0.01, compared to DHM and TGF-β1 co-treated group. AhR, aryl hydrocarbon receptor; CYP1A1, cytochrome P450 family 1 subfamily a polypeptide 1; STAT3, signal transducers and activators of transcription 3

Back to article page