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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-\u03b21 in HSCs.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      The in vivo effect of XYXD on fibrosis progression was assessed in mice model induced by carbon tetrachloride (CCl\n                      <jats:sub>4<\/jats:sub>\n                      ), The in vitro effect of XYXD on mice GFP-Col-HSC cells was evaluated using LPS and TGF-\u03b21 stimulation.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      XYXD treatment reduced CCl\n                      <jats:sub>4<\/jats:sub>\n                      -induced liver fibrosis and decreased hepatic hydroxyproline (Hyp) content, the mRNA levels of smooth muscle actin (\u03b1-SMA) and Col 1(\u03b11) in fibrotic liver. XYXD suppressed nuclear factor-\u03baB (NF-\u03baB) activation induced by LPS and TGF-\u03b21 assessed by using NF-\u03baB-luciferase reporter. The expression of NF-\u03baB 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-\u03b21 targets genes, Col1(\u03b11) and tissue inhibitor of metalloproteinases (TIMP1) induced by TGF-\u03b21 was inhibit after XYXD treatment.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>XYXD treatment attenuates liver fibrosis by inhibiting HSC activation via inhibition of NF-\u03baB and TGF-\u03b21 signaling pathway, thereby blocking the synthesis of Col1 (\u03b11) and TIMP-1. These findings from present study suggest that XYXD may be a therapeutic decoction for liver fibrosis in which NF-\u03baB and TGF-\u03b21 are thought to take part.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1186\/s12906-015-0733-1","type":"journal-article","created":{"date-parts":[[2015,6,29]],"date-time":"2015-06-29T06:18:30Z","timestamp":1435558710000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":15,"title":["RETRACTED ARTICLE: Xia-yu-xue decoction (XYXD) reduces carbon tetrachloride (CCl4)-induced liver fibrosis through inhibition hepatic stellate cell activation by targeting NF-\u03baB and TGF-\u03b21 signaling pathways"],"prefix":"10.1186","volume":"15","author":[{"given":"Cheng","family":"Liu","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Xia","family":"Yuan","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Le","family":"Tao","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Zhuoan","family":"Cheng","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Xiuqin","family":"Dai","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Xia","family":"Sheng","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Dongying","family":"Xue","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"297","published-online":{"date-parts":[[2015,6,30]]},"reference":[{"issue":"11","key":"733_CR1","doi-asserted-by":"publisher","first-page":"1324","DOI":"10.1038\/nm1663","volume":"13","author":"E Seki","year":"2007","unstructured":"Seki E, De Minicis S, Sterreicher CH, Kluwe J, Osawa Y, Brenner DA, et al. 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