Silymarin ameliorates peritoneal fibrosis by inhibiting the TGF-β/Smad signaling pathway
Abstract Peritoneal dialysis (PD) is the mainstay of treatment for renal failure replacement therapy. Although PD has greatly improved the quality of life of end-stage renal disease (ESRD) patients, long-term PD can lead to ultrafiltration failure, which in turn causes peritoneal fibrosis (PF). Sily...
Ausführliche Beschreibung
Autor*in: |
Bai, Yingwen [verfasserIn] |
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E-Artikel |
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Sprache: |
Englisch |
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2023 |
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Anmerkung: |
© The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. |
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Übergeordnetes Werk: |
Enthalten in: Naunyn-Schmiedeberg's archives of pharmacology - Berlin : Springer, 1873, 396(2023), 10 vom: 13. Apr., Seite 2379-2391 |
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Übergeordnetes Werk: |
volume:396 ; year:2023 ; number:10 ; day:13 ; month:04 ; pages:2379-2391 |
Links: |
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DOI / URN: |
10.1007/s00210-023-02450-4 |
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Katalog-ID: |
SPR053049659 |
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520 | |a Abstract Peritoneal dialysis (PD) is the mainstay of treatment for renal failure replacement therapy. Although PD has greatly improved the quality of life of end-stage renal disease (ESRD) patients, long-term PD can lead to ultrafiltration failure, which in turn causes peritoneal fibrosis (PF). Silymarin (SM) is a polyphenolic flavonoid isolated from the milk thistle (Silybum marianum) species that has a variety of pharmacological actions, including antioxidant, anti-inflammatory, antiviral, and anti-fibrotic pharmacological activities. However, the effect of SM on PF and its potential mechanisms have not been clarified. The aim of this study was to investigate the preventive effect of SM on PF in vitro and in vivo as well as elucidate the underlying mechanisms. We established PF mouse models and human pleural mesothelial cell fibrosis in vitro by intraperitoneal injection of high-glucose peritoneal dialysis solution (PDS) or transforming growth factor-β1 (TGF-β1), and evaluated the effect of SM on peritoneal fibrosis in vivo and in vitro. We found that SM alleviated peritoneal dysfunction. Meanwhile, SM inhibited the expression of fibrotic markers (TGF-β1, collagen I, fibronectin) and restored the expression of E-cadherin, BMP-7 in PF mice and TGF-β1-treated Met-5A cells. Furthermore, SM markedly down-regulated the expression of TGF-β1, p-Smad2, and p-Smad3 and up-regulated the expression of smad7. In conclusion, these findings suggested that SM may be an efficient and novel therapy for the prevention of PF through inhibition of TGF-β/Smad signaling. | ||
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650 | 4 | |a Peritoneal fibrosis |7 (dpeaa)DE-He213 | |
650 | 4 | |a TGF-β/Smad signaling pathway |7 (dpeaa)DE-He213 | |
700 | 1 | |a Wang, Lulu |4 aut | |
700 | 1 | |a Wang, Lingyun |4 aut | |
700 | 1 | |a Ge, Weihong |4 aut | |
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10.1007/s00210-023-02450-4 doi (DE-627)SPR053049659 (SPR)s00210-023-02450-4-e DE-627 ger DE-627 rakwb eng Bai, Yingwen verfasserin aut Silymarin ameliorates peritoneal fibrosis by inhibiting the TGF-β/Smad signaling pathway 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. Abstract Peritoneal dialysis (PD) is the mainstay of treatment for renal failure replacement therapy. Although PD has greatly improved the quality of life of end-stage renal disease (ESRD) patients, long-term PD can lead to ultrafiltration failure, which in turn causes peritoneal fibrosis (PF). Silymarin (SM) is a polyphenolic flavonoid isolated from the milk thistle (Silybum marianum) species that has a variety of pharmacological actions, including antioxidant, anti-inflammatory, antiviral, and anti-fibrotic pharmacological activities. However, the effect of SM on PF and its potential mechanisms have not been clarified. The aim of this study was to investigate the preventive effect of SM on PF in vitro and in vivo as well as elucidate the underlying mechanisms. We established PF mouse models and human pleural mesothelial cell fibrosis in vitro by intraperitoneal injection of high-glucose peritoneal dialysis solution (PDS) or transforming growth factor-β1 (TGF-β1), and evaluated the effect of SM on peritoneal fibrosis in vivo and in vitro. We found that SM alleviated peritoneal dysfunction. Meanwhile, SM inhibited the expression of fibrotic markers (TGF-β1, collagen I, fibronectin) and restored the expression of E-cadherin, BMP-7 in PF mice and TGF-β1-treated Met-5A cells. Furthermore, SM markedly down-regulated the expression of TGF-β1, p-Smad2, and p-Smad3 and up-regulated the expression of smad7. In conclusion, these findings suggested that SM may be an efficient and novel therapy for the prevention of PF through inhibition of TGF-β/Smad signaling. Silymarin (dpeaa)DE-He213 Peritoneal dialysis (dpeaa)DE-He213 Peritoneal fibrosis (dpeaa)DE-He213 TGF-β/Smad signaling pathway (dpeaa)DE-He213 Wang, Lulu aut Wang, Lingyun aut Ge, Weihong aut Enthalten in Naunyn-Schmiedeberg's archives of pharmacology Berlin : Springer, 1873 396(2023), 10 vom: 13. Apr., Seite 2379-2391 (DE-627)254638309 (DE-600)1462940-9 1432-1912 nnns volume:396 year:2023 number:10 day:13 month:04 pages:2379-2391 https://dx.doi.org/10.1007/s00210-023-02450-4 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 396 2023 10 13 04 2379-2391 |
spelling |
10.1007/s00210-023-02450-4 doi (DE-627)SPR053049659 (SPR)s00210-023-02450-4-e DE-627 ger DE-627 rakwb eng Bai, Yingwen verfasserin aut Silymarin ameliorates peritoneal fibrosis by inhibiting the TGF-β/Smad signaling pathway 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. Abstract Peritoneal dialysis (PD) is the mainstay of treatment for renal failure replacement therapy. Although PD has greatly improved the quality of life of end-stage renal disease (ESRD) patients, long-term PD can lead to ultrafiltration failure, which in turn causes peritoneal fibrosis (PF). Silymarin (SM) is a polyphenolic flavonoid isolated from the milk thistle (Silybum marianum) species that has a variety of pharmacological actions, including antioxidant, anti-inflammatory, antiviral, and anti-fibrotic pharmacological activities. However, the effect of SM on PF and its potential mechanisms have not been clarified. The aim of this study was to investigate the preventive effect of SM on PF in vitro and in vivo as well as elucidate the underlying mechanisms. We established PF mouse models and human pleural mesothelial cell fibrosis in vitro by intraperitoneal injection of high-glucose peritoneal dialysis solution (PDS) or transforming growth factor-β1 (TGF-β1), and evaluated the effect of SM on peritoneal fibrosis in vivo and in vitro. We found that SM alleviated peritoneal dysfunction. Meanwhile, SM inhibited the expression of fibrotic markers (TGF-β1, collagen I, fibronectin) and restored the expression of E-cadherin, BMP-7 in PF mice and TGF-β1-treated Met-5A cells. Furthermore, SM markedly down-regulated the expression of TGF-β1, p-Smad2, and p-Smad3 and up-regulated the expression of smad7. In conclusion, these findings suggested that SM may be an efficient and novel therapy for the prevention of PF through inhibition of TGF-β/Smad signaling. Silymarin (dpeaa)DE-He213 Peritoneal dialysis (dpeaa)DE-He213 Peritoneal fibrosis (dpeaa)DE-He213 TGF-β/Smad signaling pathway (dpeaa)DE-He213 Wang, Lulu aut Wang, Lingyun aut Ge, Weihong aut Enthalten in Naunyn-Schmiedeberg's archives of pharmacology Berlin : Springer, 1873 396(2023), 10 vom: 13. Apr., Seite 2379-2391 (DE-627)254638309 (DE-600)1462940-9 1432-1912 nnns volume:396 year:2023 number:10 day:13 month:04 pages:2379-2391 https://dx.doi.org/10.1007/s00210-023-02450-4 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 396 2023 10 13 04 2379-2391 |
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10.1007/s00210-023-02450-4 doi (DE-627)SPR053049659 (SPR)s00210-023-02450-4-e DE-627 ger DE-627 rakwb eng Bai, Yingwen verfasserin aut Silymarin ameliorates peritoneal fibrosis by inhibiting the TGF-β/Smad signaling pathway 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. Abstract Peritoneal dialysis (PD) is the mainstay of treatment for renal failure replacement therapy. Although PD has greatly improved the quality of life of end-stage renal disease (ESRD) patients, long-term PD can lead to ultrafiltration failure, which in turn causes peritoneal fibrosis (PF). Silymarin (SM) is a polyphenolic flavonoid isolated from the milk thistle (Silybum marianum) species that has a variety of pharmacological actions, including antioxidant, anti-inflammatory, antiviral, and anti-fibrotic pharmacological activities. However, the effect of SM on PF and its potential mechanisms have not been clarified. The aim of this study was to investigate the preventive effect of SM on PF in vitro and in vivo as well as elucidate the underlying mechanisms. We established PF mouse models and human pleural mesothelial cell fibrosis in vitro by intraperitoneal injection of high-glucose peritoneal dialysis solution (PDS) or transforming growth factor-β1 (TGF-β1), and evaluated the effect of SM on peritoneal fibrosis in vivo and in vitro. We found that SM alleviated peritoneal dysfunction. Meanwhile, SM inhibited the expression of fibrotic markers (TGF-β1, collagen I, fibronectin) and restored the expression of E-cadherin, BMP-7 in PF mice and TGF-β1-treated Met-5A cells. Furthermore, SM markedly down-regulated the expression of TGF-β1, p-Smad2, and p-Smad3 and up-regulated the expression of smad7. In conclusion, these findings suggested that SM may be an efficient and novel therapy for the prevention of PF through inhibition of TGF-β/Smad signaling. Silymarin (dpeaa)DE-He213 Peritoneal dialysis (dpeaa)DE-He213 Peritoneal fibrosis (dpeaa)DE-He213 TGF-β/Smad signaling pathway (dpeaa)DE-He213 Wang, Lulu aut Wang, Lingyun aut Ge, Weihong aut Enthalten in Naunyn-Schmiedeberg's archives of pharmacology Berlin : Springer, 1873 396(2023), 10 vom: 13. Apr., Seite 2379-2391 (DE-627)254638309 (DE-600)1462940-9 1432-1912 nnns volume:396 year:2023 number:10 day:13 month:04 pages:2379-2391 https://dx.doi.org/10.1007/s00210-023-02450-4 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 396 2023 10 13 04 2379-2391 |
allfieldsGer |
10.1007/s00210-023-02450-4 doi (DE-627)SPR053049659 (SPR)s00210-023-02450-4-e DE-627 ger DE-627 rakwb eng Bai, Yingwen verfasserin aut Silymarin ameliorates peritoneal fibrosis by inhibiting the TGF-β/Smad signaling pathway 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. Abstract Peritoneal dialysis (PD) is the mainstay of treatment for renal failure replacement therapy. Although PD has greatly improved the quality of life of end-stage renal disease (ESRD) patients, long-term PD can lead to ultrafiltration failure, which in turn causes peritoneal fibrosis (PF). Silymarin (SM) is a polyphenolic flavonoid isolated from the milk thistle (Silybum marianum) species that has a variety of pharmacological actions, including antioxidant, anti-inflammatory, antiviral, and anti-fibrotic pharmacological activities. However, the effect of SM on PF and its potential mechanisms have not been clarified. The aim of this study was to investigate the preventive effect of SM on PF in vitro and in vivo as well as elucidate the underlying mechanisms. We established PF mouse models and human pleural mesothelial cell fibrosis in vitro by intraperitoneal injection of high-glucose peritoneal dialysis solution (PDS) or transforming growth factor-β1 (TGF-β1), and evaluated the effect of SM on peritoneal fibrosis in vivo and in vitro. We found that SM alleviated peritoneal dysfunction. Meanwhile, SM inhibited the expression of fibrotic markers (TGF-β1, collagen I, fibronectin) and restored the expression of E-cadherin, BMP-7 in PF mice and TGF-β1-treated Met-5A cells. Furthermore, SM markedly down-regulated the expression of TGF-β1, p-Smad2, and p-Smad3 and up-regulated the expression of smad7. In conclusion, these findings suggested that SM may be an efficient and novel therapy for the prevention of PF through inhibition of TGF-β/Smad signaling. Silymarin (dpeaa)DE-He213 Peritoneal dialysis (dpeaa)DE-He213 Peritoneal fibrosis (dpeaa)DE-He213 TGF-β/Smad signaling pathway (dpeaa)DE-He213 Wang, Lulu aut Wang, Lingyun aut Ge, Weihong aut Enthalten in Naunyn-Schmiedeberg's archives of pharmacology Berlin : Springer, 1873 396(2023), 10 vom: 13. Apr., Seite 2379-2391 (DE-627)254638309 (DE-600)1462940-9 1432-1912 nnns volume:396 year:2023 number:10 day:13 month:04 pages:2379-2391 https://dx.doi.org/10.1007/s00210-023-02450-4 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 396 2023 10 13 04 2379-2391 |
allfieldsSound |
10.1007/s00210-023-02450-4 doi (DE-627)SPR053049659 (SPR)s00210-023-02450-4-e DE-627 ger DE-627 rakwb eng Bai, Yingwen verfasserin aut Silymarin ameliorates peritoneal fibrosis by inhibiting the TGF-β/Smad signaling pathway 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. Abstract Peritoneal dialysis (PD) is the mainstay of treatment for renal failure replacement therapy. Although PD has greatly improved the quality of life of end-stage renal disease (ESRD) patients, long-term PD can lead to ultrafiltration failure, which in turn causes peritoneal fibrosis (PF). Silymarin (SM) is a polyphenolic flavonoid isolated from the milk thistle (Silybum marianum) species that has a variety of pharmacological actions, including antioxidant, anti-inflammatory, antiviral, and anti-fibrotic pharmacological activities. However, the effect of SM on PF and its potential mechanisms have not been clarified. The aim of this study was to investigate the preventive effect of SM on PF in vitro and in vivo as well as elucidate the underlying mechanisms. We established PF mouse models and human pleural mesothelial cell fibrosis in vitro by intraperitoneal injection of high-glucose peritoneal dialysis solution (PDS) or transforming growth factor-β1 (TGF-β1), and evaluated the effect of SM on peritoneal fibrosis in vivo and in vitro. We found that SM alleviated peritoneal dysfunction. Meanwhile, SM inhibited the expression of fibrotic markers (TGF-β1, collagen I, fibronectin) and restored the expression of E-cadherin, BMP-7 in PF mice and TGF-β1-treated Met-5A cells. Furthermore, SM markedly down-regulated the expression of TGF-β1, p-Smad2, and p-Smad3 and up-regulated the expression of smad7. In conclusion, these findings suggested that SM may be an efficient and novel therapy for the prevention of PF through inhibition of TGF-β/Smad signaling. Silymarin (dpeaa)DE-He213 Peritoneal dialysis (dpeaa)DE-He213 Peritoneal fibrosis (dpeaa)DE-He213 TGF-β/Smad signaling pathway (dpeaa)DE-He213 Wang, Lulu aut Wang, Lingyun aut Ge, Weihong aut Enthalten in Naunyn-Schmiedeberg's archives of pharmacology Berlin : Springer, 1873 396(2023), 10 vom: 13. Apr., Seite 2379-2391 (DE-627)254638309 (DE-600)1462940-9 1432-1912 nnns volume:396 year:2023 number:10 day:13 month:04 pages:2379-2391 https://dx.doi.org/10.1007/s00210-023-02450-4 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 396 2023 10 13 04 2379-2391 |
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Enthalten in Naunyn-Schmiedeberg's archives of pharmacology 396(2023), 10 vom: 13. Apr., Seite 2379-2391 volume:396 year:2023 number:10 day:13 month:04 pages:2379-2391 |
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Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Abstract Peritoneal dialysis (PD) is the mainstay of treatment for renal failure replacement therapy. Although PD has greatly improved the quality of life of end-stage renal disease (ESRD) patients, long-term PD can lead to ultrafiltration failure, which in turn causes peritoneal fibrosis (PF). Silymarin (SM) is a polyphenolic flavonoid isolated from the milk thistle (Silybum marianum) species that has a variety of pharmacological actions, including antioxidant, anti-inflammatory, antiviral, and anti-fibrotic pharmacological activities. However, the effect of SM on PF and its potential mechanisms have not been clarified. The aim of this study was to investigate the preventive effect of SM on PF in vitro and in vivo as well as elucidate the underlying mechanisms. We established PF mouse models and human pleural mesothelial cell fibrosis in vitro by intraperitoneal injection of high-glucose peritoneal dialysis solution (PDS) or transforming growth factor-β1 (TGF-β1), and evaluated the effect of SM on peritoneal fibrosis in vivo and in vitro. We found that SM alleviated peritoneal dysfunction. Meanwhile, SM inhibited the expression of fibrotic markers (TGF-β1, collagen I, fibronectin) and restored the expression of E-cadherin, BMP-7 in PF mice and TGF-β1-treated Met-5A cells. Furthermore, SM markedly down-regulated the expression of TGF-β1, p-Smad2, and p-Smad3 and up-regulated the expression of smad7. 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Bai, Yingwen |
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Bai, Yingwen misc Silymarin misc Peritoneal dialysis misc Peritoneal fibrosis misc TGF-β/Smad signaling pathway Silymarin ameliorates peritoneal fibrosis by inhibiting the TGF-β/Smad signaling pathway |
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Silymarin ameliorates peritoneal fibrosis by inhibiting the TGF-β/Smad signaling pathway Silymarin (dpeaa)DE-He213 Peritoneal dialysis (dpeaa)DE-He213 Peritoneal fibrosis (dpeaa)DE-He213 TGF-β/Smad signaling pathway (dpeaa)DE-He213 |
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Silymarin ameliorates peritoneal fibrosis by inhibiting the TGF-β/Smad signaling pathway |
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Silymarin ameliorates peritoneal fibrosis by inhibiting the TGF-β/Smad signaling pathway |
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Bai, Yingwen |
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silymarin ameliorates peritoneal fibrosis by inhibiting the tgf-β/smad signaling pathway |
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Silymarin ameliorates peritoneal fibrosis by inhibiting the TGF-β/Smad signaling pathway |
abstract |
Abstract Peritoneal dialysis (PD) is the mainstay of treatment for renal failure replacement therapy. Although PD has greatly improved the quality of life of end-stage renal disease (ESRD) patients, long-term PD can lead to ultrafiltration failure, which in turn causes peritoneal fibrosis (PF). Silymarin (SM) is a polyphenolic flavonoid isolated from the milk thistle (Silybum marianum) species that has a variety of pharmacological actions, including antioxidant, anti-inflammatory, antiviral, and anti-fibrotic pharmacological activities. However, the effect of SM on PF and its potential mechanisms have not been clarified. The aim of this study was to investigate the preventive effect of SM on PF in vitro and in vivo as well as elucidate the underlying mechanisms. We established PF mouse models and human pleural mesothelial cell fibrosis in vitro by intraperitoneal injection of high-glucose peritoneal dialysis solution (PDS) or transforming growth factor-β1 (TGF-β1), and evaluated the effect of SM on peritoneal fibrosis in vivo and in vitro. We found that SM alleviated peritoneal dysfunction. Meanwhile, SM inhibited the expression of fibrotic markers (TGF-β1, collagen I, fibronectin) and restored the expression of E-cadherin, BMP-7 in PF mice and TGF-β1-treated Met-5A cells. Furthermore, SM markedly down-regulated the expression of TGF-β1, p-Smad2, and p-Smad3 and up-regulated the expression of smad7. In conclusion, these findings suggested that SM may be an efficient and novel therapy for the prevention of PF through inhibition of TGF-β/Smad signaling. © The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. |
abstractGer |
Abstract Peritoneal dialysis (PD) is the mainstay of treatment for renal failure replacement therapy. Although PD has greatly improved the quality of life of end-stage renal disease (ESRD) patients, long-term PD can lead to ultrafiltration failure, which in turn causes peritoneal fibrosis (PF). Silymarin (SM) is a polyphenolic flavonoid isolated from the milk thistle (Silybum marianum) species that has a variety of pharmacological actions, including antioxidant, anti-inflammatory, antiviral, and anti-fibrotic pharmacological activities. However, the effect of SM on PF and its potential mechanisms have not been clarified. The aim of this study was to investigate the preventive effect of SM on PF in vitro and in vivo as well as elucidate the underlying mechanisms. We established PF mouse models and human pleural mesothelial cell fibrosis in vitro by intraperitoneal injection of high-glucose peritoneal dialysis solution (PDS) or transforming growth factor-β1 (TGF-β1), and evaluated the effect of SM on peritoneal fibrosis in vivo and in vitro. We found that SM alleviated peritoneal dysfunction. Meanwhile, SM inhibited the expression of fibrotic markers (TGF-β1, collagen I, fibronectin) and restored the expression of E-cadherin, BMP-7 in PF mice and TGF-β1-treated Met-5A cells. Furthermore, SM markedly down-regulated the expression of TGF-β1, p-Smad2, and p-Smad3 and up-regulated the expression of smad7. In conclusion, these findings suggested that SM may be an efficient and novel therapy for the prevention of PF through inhibition of TGF-β/Smad signaling. © The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. |
abstract_unstemmed |
Abstract Peritoneal dialysis (PD) is the mainstay of treatment for renal failure replacement therapy. Although PD has greatly improved the quality of life of end-stage renal disease (ESRD) patients, long-term PD can lead to ultrafiltration failure, which in turn causes peritoneal fibrosis (PF). Silymarin (SM) is a polyphenolic flavonoid isolated from the milk thistle (Silybum marianum) species that has a variety of pharmacological actions, including antioxidant, anti-inflammatory, antiviral, and anti-fibrotic pharmacological activities. However, the effect of SM on PF and its potential mechanisms have not been clarified. The aim of this study was to investigate the preventive effect of SM on PF in vitro and in vivo as well as elucidate the underlying mechanisms. We established PF mouse models and human pleural mesothelial cell fibrosis in vitro by intraperitoneal injection of high-glucose peritoneal dialysis solution (PDS) or transforming growth factor-β1 (TGF-β1), and evaluated the effect of SM on peritoneal fibrosis in vivo and in vitro. We found that SM alleviated peritoneal dysfunction. Meanwhile, SM inhibited the expression of fibrotic markers (TGF-β1, collagen I, fibronectin) and restored the expression of E-cadherin, BMP-7 in PF mice and TGF-β1-treated Met-5A cells. Furthermore, SM markedly down-regulated the expression of TGF-β1, p-Smad2, and p-Smad3 and up-regulated the expression of smad7. In conclusion, these findings suggested that SM may be an efficient and novel therapy for the prevention of PF through inhibition of TGF-β/Smad signaling. © The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. |
collection_details |
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title_short |
Silymarin ameliorates peritoneal fibrosis by inhibiting the TGF-β/Smad signaling pathway |
url |
https://dx.doi.org/10.1007/s00210-023-02450-4 |
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Wang, Lulu Wang, Lingyun Ge, Weihong |
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up_date |
2024-07-03T16:42:08.562Z |
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score |
7.3985195 |