Qinggan Huoxue Recipe suppresses epithelial-to-mesenchymal transition in alcoholic liver fibrosis through TGF-β1/Smad signaling pathway

Wu, Tao; Chen, Junming; Xiao, Tiegang; Shu, Xiangbing; Xu, Hanchen; Yang, Lili; Xing, Lian-Jun; Zheng, Peiyong; Ji, Guang

doi:10.3748/wjg.v22.i19.4695

Cited by 28 publications

(15 citation statements)

References 28 publications

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“…In our study, the compound treatment significantly decreased relative mRNA and/or protein expression levels of hepatic TGF- β 1, (phospho-)Smad2, and (phospho-)Smad3 but increased the Smad7 expression. The changes of TGF- β 1 and Smads are consistent with previous studies about the molecular mechanism of liver fibrosis [39–41], suggesting that the protective effect of the compound is via TGF- β 1/Smad signaling pathway.…”

Section: Discussionsupporting

confidence: 90%

A Compound of Chinese Herbs Protects against Alcoholic Liver Fibrosis in Rats via the TGF-β1/Smad Signaling Pathway

Liu

Yue

et al. 2019

Evidence-Based Complementary and Alternative Medicine

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Alcoholic liver fibrosis (ALF) has become a major public health concern owing to its health impacts and the lack of effective treatment strategies for the disease. In this study, we investigated the effect of a compound composed of Chinese herbs Pueraria lobata (Willd.), Salvia miltiorrhiza, Schisandra chinensis, and Silybum marianum on ALF. An ALF model was established. Rats were fed with modified Lieber–Decarli alcohol liquid diet and injected with trace CCl4 at late stage. The rats were then treated with several doses of the compound. Biochemical and fibrosis-relevant parameters were measured from the sera obtained from the rats. Liver tissues were obtained for hematoxylin and eosin and Masson’s trichrome staining. Matrix metalloproteinase-13 and tissue inhibitor of metalloproteinase-1 were determined by immunohistochemistry assays. The mRNA and protein expression levels of transforming growth factor-β1 (TGF-β1), Smad2, Smad3, and Smad7 on the livers were also measured by quantitative polymerase chain reaction and Western blot. Results showed that the compound treatment alleviated pathological lesions in the liver, decreased the serum levels of hyaluronan, laminin, and hydroxyproline, and diminished the expression of hepatic tissue inhibitor of metalloproteinase-1. Compound treatment also increased hepatic matrix metalloproteinase-13 expression and inhibited the TGF-β1/Smad signaling pathway. In conclusion, the compound has a protective effect against ALF in rats, and an underlying mechanism is involved in the TGF-β1/Smad signaling pathway.

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Section: Discussionsupporting

confidence: 90%

A Compound of Chinese Herbs Protects against Alcoholic Liver Fibrosis in Rats via the TGF-β1/Smad Signaling Pathway

Liu

Yue

et al. 2019

Evidence-Based Complementary and Alternative Medicine

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“…In schistosome-induced liver damage, abnormal SOD expression was found to promote liver fibrosis [ 31 , 32 ]. In a previous study, it was shown that serum HA levels were significantly increased in rat liver fibrosis [ 33 , 34 ]. In the present study, we showed that S. japonicum infection induced serum HA levels and reduced SOD activities in the liver.…”

Section: Discussionmentioning

confidence: 99%

A Polysaccharide from Amusium Pleuronectes Combined with Praziquantel Treatment Ameliorates Hepatic Fibrosis in Schistosoma Japonicum-Infected Mice

Tang

et al. 2018

Med Sci Monit

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BackgroundPolysaccharides from bivalves have multiple bioactivities in various aspects of biology. However, the role of a polysaccharide derived from Amusium pleuronectes on potential hepatoprotective effects remains unclear.Material/MethodsA water-soluble polysaccharide was isolated from Amusium pleuronectes (APS-1) using ultrasound-assisted hot-water extraction. The molecular weight of APS-1 was approximately 11.7 kDa and was determined by calibration with dextran. APS-1 was analyzed by high-performance liquid chromatography (HPLC), and mainly consisted of a uniform glucose polymer. The protective effect of APS-1 on Schistosoma japonicum-induced liver fibrosis was investigated in a mouse model.ResultsTreatment with APS-1 increased serum levels of interleukin (IL)-12 and interferon (IFN)-γ, increased superoxide dismutase (SOD) activity, and decreased levels of IL-13 and IL-5, and hyaluronidase activity. Moreover, immunohistochemical analysis revealed that the collagen content of hepatic tissue of APS-1-treated mice, including that of collagen I, II, and IV, was dramatically decreased. Furthermore, our data showed that combined treatment of APS-1 with praziquantel had more pronounced effects than treatment with either APS-1 or praziquantel alone.ConclusionsOur findings suggest that the treatment using APS-1 in combination with praziquantel attenuated S. japonicum egg-induced hepatic fibrosis, and possessed potent hepatoprotective activity.

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“…Any chronic form of hepatic injury can result in the transformation of hepatocytes into mesenchymal cells by an epithelial–mesenchymal transition (EMT) process. EMT is a dynamic program in which fully differentiated epithelial cells undergo a phenotypic change, resulting in loss of marker proteins such as E-cadherin and zonula occludens-1 (ZO-1), and acquisition of mesenchymal characteristics such as α-SMA, vimentin, matrix metalloproteinase (MMP)-2, MMP-9, and collagens [ 7 , 8 ]. In addition, following damage to the epithelial cells, bile-duct epithelium and hepatocytes released the profibrogenic cytokine that further activates HSCs [ 9 , 10 ].…”

Section: Introductionmentioning

confidence: 99%

“…Many studies have identified that a variety of cytokines and growth factors, including transforming growth factor-β1 (TGF-β1), epidermal growth factor (EGF), and hepatocyte growth factor (HGF), participate in the EMT process [ 7 , 15 , 16 ]. TGF-β1/Smad signaling has been reported as a mechanism leading to hepatic fibrosis.…”

Section: Introductionmentioning

confidence: 99%

Antifibrotic Effect of Smad Decoy Oligodeoxynucleotide in a CCl4-Induced Hepatic Fibrosis Animal Model

Gwon

Kim

et al. 2018

Molecules

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Hepatic fibrosis is the wound-healing process of chronic hepatic disease that leads to the end-stage of hepatocellular carcinoma and demolition of hepatic structures. Epithelial–mesenchymal transition (EMT) has been identified to phenotypic conversion of the epithelium to mesenchymal phenotype that occurred during fibrosis. Smad decoy oligodeoxynucleotide (ODN) is a synthetic DNA fragment containing a complementary sequence of Smad transcription factor. Thus, this study evaluated the antifibrotic effects of Smad decoy ODN on carbon tetrachloride (CCl4)-induced hepatic fibrosis in mice. As shown in histological results, CCl4 treatment triggered hepatic fibrosis and increased Smad expression. On the contrary, Smad decoy ODN administration suppressed fibrogenesis and EMT process. The expression of Smad signaling and EMT-associated protein was markedly decreased in Smad decoy ODN-treated mice compared with CCl4-injured mice. In conclusion, these data indicate the practicability of Smad decoy ODN administration for preventing hepatic fibrosis and EMT processes.

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Qinggan Huoxue Recipe suppresses epithelial-to-mesenchymal transition in alcoholic liver fibrosis through TGF-β1/Smad signaling pathway

Abstract: Qinggan Huoxue Recipe inhibits EMT in ALF rats by modulating the TGF-β1/Smad signaling pathway, suggesting that the mechanism underlying the amelioration of ALF induced by QGHXR is associated with this pathway.

Cited by 28 publications

References 28 publications

A Compound of Chinese Herbs Protects against Alcoholic Liver Fibrosis in Rats via the TGF-β1/Smad Signaling Pathway

A Compound of Chinese Herbs Protects against Alcoholic Liver Fibrosis in Rats via the TGF-β1/Smad Signaling Pathway

A Polysaccharide from Amusium Pleuronectes Combined with Praziquantel Treatment Ameliorates Hepatic Fibrosis in Schistosoma Japonicum-Infected Mice

Antifibrotic Effect of Smad Decoy Oligodeoxynucleotide in a CCl4-Induced Hepatic Fibrosis Animal Model

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