RETRACTED ARTICLE: Xia-yu-xue decoction (XYXD) reduces carbon tetrachloride (CCl4)-induced liver fibrosis through inhibition hepatic stellate cell activation by targeting NF-κB and TGF-β1 signaling pathways
Liver Cirrhosis
2. Zero hunger
NF-kappa B
3. Good health
Transforming Growth Factor beta1
Mice
Complementary and alternative medicine
Hepatic Stellate Cells
Animals
Carbon Tetrachloride
Cells, Cultured
Research Article
Drugs, Chinese Herbal
Signal Transduction
DOI:
10.1186/s12906-015-0733-1
Publication Date:
2015-06-29T10:18:30Z
AUTHORS (7)
ABSTRACT
Abstract
Background
Hepatic stellate cell (HSC) activation is activated mainly by endotoxin and transforming growth factor (TGF-β1) in chronic liver injury, consequently, can be important therapeutic targets. Xia-yu-xue decoction (XYXD), a classical recipe used in China to treat liver fibrosis, and has been revealed to inhibit hepatic fibrosis in animal models, the mechanism of action of XYXD remains elusive. In the present study, we evaluated whether XYXD reduced endotoxin and pro-fibrogenic pathways induced by lipopolysaccharide (LPS) and TGF-β1 in HSCs.
Methods
The in vivo effect of XYXD on fibrosis progression was assessed in mice model induced by carbon tetrachloride (CCl4), The in vitro effect of XYXD on mice GFP-Col-HSC cells was evaluated using LPS and TGF-β1 stimulation.
Results
XYXD treatment reduced CCl4-induced liver fibrosis and decreased hepatic hydroxyproline (Hyp) content, the mRNA levels of smooth muscle actin (α-SMA) and Col 1(α1) in fibrotic liver. XYXD suppressed nuclear factor-κB (NF-κB) activation induced by LPS and TGF-β1 assessed by using NF-κB-luciferase reporter. The expression of NF-κB target genes, chemokine (C-C motif) ligand 2 (CCL2) and chemokine (C-X-C motif) ligand 2 (CXCL2) induced by LPS was suppressed after XYXD treatment. The expression of TGF-β1 targets genes, Col1(α1) and tissue inhibitor of metalloproteinases (TIMP1) induced by TGF-β1 was inhibit after XYXD treatment.
Conclusion
XYXD treatment attenuates liver fibrosis by inhibiting HSC activation via inhibition of NF-κB and TGF-β1 signaling pathway, thereby blocking the synthesis of Col1 (α1) and TIMP-1. These findings from present study suggest that XYXD may be a therapeutic decoction for liver fibrosis in which NF-κB and TGF-β1 are thought to take part.
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