BMC complementary and alternative medicine · 2015
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.
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СтатьяПоддержка исследования: вне правительства СШАОтозванная публикацияНазвание и аннотация: Перевод в очереди
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Liu Cheng, Yuan Xia, Tao Le, Cheng Zhuoan, Dai Xiuqin, Sheng Xia, Xue Dongying
Аннотация
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.
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.