Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2016 Dec 29;15(2):613–626. doi: 10.3892/mmr.2016.6083

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

Copyright: © Xiang et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

PMC Copyright notice

Figure 3. — DMN, YGD and HGF regulate the expression of α-SMA, CXCR4, ERK1/2, NF-κB p65 and β-catenin. Mice were injected with DMN or normal saline for 4 weeks. Following 4 weeks of DMN treatment, mice were treated with YGD or HGF for a further 4 weeks. Liver sections were stained for (A) α-SMA (B) CXCR4. (C) ERK1/2 (D) NF-κB p65. (E) β-catenin. A representative image from each group is presented. Very little staining was observed in the control group. YGD or HGF treatment increased CXCR4 and ERK1/2 staining, and decreased α-SMA, NF-κB p65 and β-catenin staining, compared with the DMN-injected group. Magnification, ×400; scale bar=50 µm.YGD, Yi Guan Jian decoction; HGF, hepatocyte growth factor; DMN, dimethylnitrosamine; α-SMA, α-smooth muscle actin; CXCR4, C-X-C chemokine receptor type 4; ERK1/2, extracellular signal-regulated kinase 1/2; NF-κB p65, nuclear factor κB p65 subunit; C, control; M, model; NC, negative control; W, week.

Figure 3. — DMN, YGD and HGF regulate the expression of α-SMA, CXCR4, ERK1/2, NF-κB p65 and β-catenin. Mice were injected with DMN or normal saline for 4 weeks. Following 4 weeks of DMN treatment, mice were treated with YGD or HGF for a further 4 weeks. Liver sections were stained for (A) α-SMA (B) CXCR4. (C) ERK1/2 (D) NF-κB p65. (E) β-catenin. A representative image from each group is presented. Very little staining was observed in the control group. YGD or HGF treatment increased CXCR4 and ERK1/2 staining, and decreased α-SMA, NF-κB p65 and β-catenin staining, compared with the DMN-injected group. Magnification, ×400; scale bar=50 µm.YGD, Yi Guan Jian decoction; HGF, hepatocyte growth factor; DMN, dimethylnitrosamine; α-SMA, α-smooth muscle actin; CXCR4, C-X-C chemokine receptor type 4; ERK1/2, extracellular signal-regulated kinase 1/2; NF-κB p65, nuclear factor κB p65 subunit; C, control; M, model; NC, negative control; W, week.