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Ingredients of Huangqi decoction slow biliary fibrosis progression by inhibiting the activation of the transforming growth factor-beta signaling pathway

BACKGROUND: Huangqi decoction was first described in Prescriptions of the Bureau of Taiping People's Welfare Pharmacy in Song Dynasty (AD 1078), and it is an effective recipe that is usually used to treat consumptive disease, anorexia, and chronic liver diseases. Transforming growth factor beta...

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Autores principales: Du, Jin-Xing, Sun, Ming-Yu, Du, Guang-Li, Li, Feng-Hua, Liu, Cheng, Mu, Yong-Ping, Chen, Gao-Feng, Long, Ai-Hua, Bian, Yan-Qin, Liu, Jia, Liu, Cheng-Hai, Hu, Yi-Yang, Xu, Lie-Ming, Liu, Ping
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3419610/
https://www.ncbi.nlm.nih.gov/pubmed/22471627
http://dx.doi.org/10.1186/1472-6882-12-33
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author Du, Jin-Xing
Sun, Ming-Yu
Du, Guang-Li
Li, Feng-Hua
Liu, Cheng
Mu, Yong-Ping
Chen, Gao-Feng
Long, Ai-Hua
Bian, Yan-Qin
Liu, Jia
Liu, Cheng-Hai
Hu, Yi-Yang
Xu, Lie-Ming
Liu, Ping
author_facet Du, Jin-Xing
Sun, Ming-Yu
Du, Guang-Li
Li, Feng-Hua
Liu, Cheng
Mu, Yong-Ping
Chen, Gao-Feng
Long, Ai-Hua
Bian, Yan-Qin
Liu, Jia
Liu, Cheng-Hai
Hu, Yi-Yang
Xu, Lie-Ming
Liu, Ping
author_sort Du, Jin-Xing
collection PubMed
description BACKGROUND: Huangqi decoction was first described in Prescriptions of the Bureau of Taiping People's Welfare Pharmacy in Song Dynasty (AD 1078), and it is an effective recipe that is usually used to treat consumptive disease, anorexia, and chronic liver diseases. Transforming growth factor beta 1 (TGFβ1) plays a key role in the progression of liver fibrosis, and Huangqi decoction and its ingredients (IHQD) markedly ameliorated hepatic fibrotic lesions induced by ligation of the common bile duct (BDL). However, the mechanism of IHQD on hepatic fibrotic lesions is not yet clear. The purpose of the present study is to elucidate the roles of TGFβ1 activation, Smad-signaling pathway, and extracellular signal-regulated kinase (ERK) in the pathogenesis of biliary fibrosis progression and the antifibrotic mechanism of IHQD. METHODS: A liver fibrosis model was induced by ligation of the common bile duct (BDL) in rats. Sham-operation was performed in control rats. The BDL rats were randomly divided into two groups: the BDL group and the IHQD group. IHQD was administrated intragastrically for 4 weeks. At the end of the fifth week after BDL, animals were sacrificed for sampling of blood serum and liver tissue. The effect of IHQD on the TGFβ1 signaling pathway was evaluated by western blotting and laser confocal microscopy. RESULTS: Decreased content of hepatic hydroxyproline and improved liver function and histopathology were observed in IHQD rats. Hepatocytes, cholangiocytes, and myofibroblasts in the cholestatic liver injury released TGFβ1, and activated TGFβ1 receptors can accelerate liver fibrosis. IHQD markedly inhibited the protein expression of TGFβ1, TGFβ1 receptors, Smad3, and p-ERK1/2 expression with no change of Smad7 expression. CONCLUSION: IHQD exert significant therapeutic effects on BDL-induced fibrosis in rats through inhibition of the activation of TGFβ1-Smad3 and TGFβ1-ERK1/2 signaling pathways.
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spelling pubmed-34196102012-08-16 Ingredients of Huangqi decoction slow biliary fibrosis progression by inhibiting the activation of the transforming growth factor-beta signaling pathway Du, Jin-Xing Sun, Ming-Yu Du, Guang-Li Li, Feng-Hua Liu, Cheng Mu, Yong-Ping Chen, Gao-Feng Long, Ai-Hua Bian, Yan-Qin Liu, Jia Liu, Cheng-Hai Hu, Yi-Yang Xu, Lie-Ming Liu, Ping BMC Complement Altern Med Research Article BACKGROUND: Huangqi decoction was first described in Prescriptions of the Bureau of Taiping People's Welfare Pharmacy in Song Dynasty (AD 1078), and it is an effective recipe that is usually used to treat consumptive disease, anorexia, and chronic liver diseases. Transforming growth factor beta 1 (TGFβ1) plays a key role in the progression of liver fibrosis, and Huangqi decoction and its ingredients (IHQD) markedly ameliorated hepatic fibrotic lesions induced by ligation of the common bile duct (BDL). However, the mechanism of IHQD on hepatic fibrotic lesions is not yet clear. The purpose of the present study is to elucidate the roles of TGFβ1 activation, Smad-signaling pathway, and extracellular signal-regulated kinase (ERK) in the pathogenesis of biliary fibrosis progression and the antifibrotic mechanism of IHQD. METHODS: A liver fibrosis model was induced by ligation of the common bile duct (BDL) in rats. Sham-operation was performed in control rats. The BDL rats were randomly divided into two groups: the BDL group and the IHQD group. IHQD was administrated intragastrically for 4 weeks. At the end of the fifth week after BDL, animals were sacrificed for sampling of blood serum and liver tissue. The effect of IHQD on the TGFβ1 signaling pathway was evaluated by western blotting and laser confocal microscopy. RESULTS: Decreased content of hepatic hydroxyproline and improved liver function and histopathology were observed in IHQD rats. Hepatocytes, cholangiocytes, and myofibroblasts in the cholestatic liver injury released TGFβ1, and activated TGFβ1 receptors can accelerate liver fibrosis. IHQD markedly inhibited the protein expression of TGFβ1, TGFβ1 receptors, Smad3, and p-ERK1/2 expression with no change of Smad7 expression. CONCLUSION: IHQD exert significant therapeutic effects on BDL-induced fibrosis in rats through inhibition of the activation of TGFβ1-Smad3 and TGFβ1-ERK1/2 signaling pathways. BioMed Central 2012-04-03 /pmc/articles/PMC3419610/ /pubmed/22471627 http://dx.doi.org/10.1186/1472-6882-12-33 Text en Copyright ©2012 Du et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Du, Jin-Xing
Sun, Ming-Yu
Du, Guang-Li
Li, Feng-Hua
Liu, Cheng
Mu, Yong-Ping
Chen, Gao-Feng
Long, Ai-Hua
Bian, Yan-Qin
Liu, Jia
Liu, Cheng-Hai
Hu, Yi-Yang
Xu, Lie-Ming
Liu, Ping
Ingredients of Huangqi decoction slow biliary fibrosis progression by inhibiting the activation of the transforming growth factor-beta signaling pathway
title Ingredients of Huangqi decoction slow biliary fibrosis progression by inhibiting the activation of the transforming growth factor-beta signaling pathway
title_full Ingredients of Huangqi decoction slow biliary fibrosis progression by inhibiting the activation of the transforming growth factor-beta signaling pathway
title_fullStr Ingredients of Huangqi decoction slow biliary fibrosis progression by inhibiting the activation of the transforming growth factor-beta signaling pathway
title_full_unstemmed Ingredients of Huangqi decoction slow biliary fibrosis progression by inhibiting the activation of the transforming growth factor-beta signaling pathway
title_short Ingredients of Huangqi decoction slow biliary fibrosis progression by inhibiting the activation of the transforming growth factor-beta signaling pathway
title_sort ingredients of huangqi decoction slow biliary fibrosis progression by inhibiting the activation of the transforming growth factor-beta signaling pathway
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3419610/
https://www.ncbi.nlm.nih.gov/pubmed/22471627
http://dx.doi.org/10.1186/1472-6882-12-33
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