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. 2018 Jun 22;12:1837–1853. doi: 10.2147/DDDT.S162950

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© 2018 Feng et al. This work is published and licensed by Dove Medical Press Limited

The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

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Salidroside inhibited the TGF-β1/Smad3 pathway in liver fibrosis.

Notes: (A) Western blot and quantitative analyses of TGF-β1/Smad3 pathway. Salidroside inhibited the expression of these proteins in both liver fibrosis mouse models. (B) The qPCR analyses. Salidroside attenuated TGF-β1 mRNA expression. (C) Immunohistochemical staining showed that salidroside reduced the expression of TGF-β1 and p-Smad3 in liver tissues in both model groups (original magnification, ×200, scale bar =100 μm). (D) Representative images of double-immunofluorescence staining of liver sections were showed here (original magnification, ×400). α-SMA is considered to be a marker of activated HSCs, and F4/80 is the specific marker of KCs. There were positive areas in CCl₄ and BDL groups. However, salidroside treatment could effectively inhibit the expression of TGF-β1 in these two kinds of cells. Data were given as mean ± SD (n=8, *P<0.05 for CCl₄ or BDL group vs vehicle or sham group, ^#P<0.05 for CCl₄ + Sal 10 mg/kg or BDL + Sal 10 mg/kg vs CCl₄ or BDL group, and ⁺P<0.05 for CCl₄ + Sal 20 mg/kg or BDL + Sal 20 mg/kg vs CCl₄ + Sal 10 mg/kg or BDL + Sal 10 mg/kg).

Abbreviations: BDL, bile duct ligation; CCl₄, carbon tetrachloride; HSCs, hepatic stellate cells; KCs, Kupffer cells; qPCR, quantitative real-time polymerase chain reaction; Sal, salidroside; SD, standard deviation.

Salidroside inhibited the TGF-β1/Smad3 pathway in liver fibrosis.

Notes: (A) Western blot and quantitative analyses of TGF-β1/Smad3 pathway. Salidroside inhibited the expression of these proteins in both liver fibrosis mouse models. (B) The qPCR analyses. Salidroside attenuated TGF-β1 mRNA expression. (C) Immunohistochemical staining showed that salidroside reduced the expression of TGF-β1 and p-Smad3 in liver tissues in both model groups (original magnification, ×200, scale bar =100 μm). (D) Representative images of double-immunofluorescence staining of liver sections were showed here (original magnification, ×400). α-SMA is considered to be a marker of activated HSCs, and F4/80 is the specific marker of KCs. There were positive areas in CCl₄ and BDL groups. However, salidroside treatment could effectively inhibit the expression of TGF-β1 in these two kinds of cells. Data were given as mean ± SD (n=8, *P<0.05 for CCl₄ or BDL group vs vehicle or sham group, ^#P<0.05 for CCl₄ + Sal 10 mg/kg or BDL + Sal 10 mg/kg vs CCl₄ or BDL group, and ⁺P<0.05 for CCl₄ + Sal 20 mg/kg or BDL + Sal 20 mg/kg vs CCl₄ + Sal 10 mg/kg or BDL + Sal 10 mg/kg).

Abbreviations: BDL, bile duct ligation; CCl₄, carbon tetrachloride; HSCs, hepatic stellate cells; KCs, Kupffer cells; qPCR, quantitative real-time polymerase chain reaction; Sal, salidroside; SD, standard deviation.