Salvianolic acid B inhibits the progression of liver fibrosis in rats via modulation of the Hedgehog signaling pathway
Salvianolic acid B (Sal B) has previously reported anti-hepatic fibrosis effects, though it is not clear if it can inhibit hepatic fibrosis by regulating the hedgehog (Hh) signaling pathway. The aim of the present study was to explore the roles and mechanism of Sal B in preventing and treating liver...
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| Veröffentlicht in: | Experimental and therapeutic medicine 2022-02, Vol.23 (2), p.116, Article 116 |
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| creator | Tao, Shanjun Duan, Renjie Xu, Tong Hong, Jiao Gu, Wenjie Lin, Aiqin Lian, Likai Huang, Haoyu Lu, Jiangtao Li, Tiechen |
| description | Salvianolic acid B (Sal B) has previously reported anti-hepatic fibrosis effects, though it is not clear if it can inhibit hepatic fibrosis by regulating the hedgehog (Hh) signaling pathway. The aim of the present study was to explore the roles and mechanism of Sal B in preventing and treating liver fibrosis in rats. The study also aimed to determine the role of the Hh signaling pathway in this process. A rat model of liver fibrosis was induced through the subcutaneous injection of 50% carbon tetrachloride, followed by treatment with Sal B. After gavage, blood was collected to detect serum markers of liver injury. The degree of liver fibrosis and tissue damage was assessed using histopathological analysis. Western blotting and reverse transcription-quantitative PCR were used to detect the expression levels of TGF-β1 and Hh signaling pathway-related genes, including Sonic hedgehog (Shh) protein, membrane protein receptor protein patched homolog 1 (Ptch1), membrane protein receptor Smoothened (Smo) and transcription factor glioma-associated oncogene homolog 1 (Gli1). Serum alanine aminotransferase, aspartate aminotransferase and total bilirubin levels were decreased, whilst levels of albumin were increased in rats with liver fibrosis that were treated with Sal B (P |
| doi_str_mv | 10.3892/etm.2021.11039 |
| format | Article |
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The aim of the present study was to explore the roles and mechanism of Sal B in preventing and treating liver fibrosis in rats. The study also aimed to determine the role of the Hh signaling pathway in this process. A rat model of liver fibrosis was induced through the subcutaneous injection of 50% carbon tetrachloride, followed by treatment with Sal B. After gavage, blood was collected to detect serum markers of liver injury. The degree of liver fibrosis and tissue damage was assessed using histopathological analysis. Western blotting and reverse transcription-quantitative PCR were used to detect the expression levels of TGF-β1 and Hh signaling pathway-related genes, including Sonic hedgehog (Shh) protein, membrane protein receptor protein patched homolog 1 (Ptch1), membrane protein receptor Smoothened (Smo) and transcription factor glioma-associated oncogene homolog 1 (Gli1). Serum alanine aminotransferase, aspartate aminotransferase and total bilirubin levels were decreased, whilst levels of albumin were increased in rats with liver fibrosis that were treated with Sal B (P<0.05). Additionally, significant increases in TGF-β1, Shh, Ptch1, Smo, Gli1 and α-smooth muscle actin expression levels were observed in the liver tissues of rats with hepatic fibrosis (P<0.05). However, Sal B treatment significantly reduced the expression levels of these proteins (P<0.05). In conclusion, the results of the present study suggested that the Hh signaling pathway may be activated during the process of rat liver fibrosis. Thus, Sal B may exert its anti-hepatic fibrosis effects, at least in part, by inhibiting the activation of the Hh signaling pathway.</description><identifier>ISSN: 1792-0981</identifier><identifier>EISSN: 1792-1015</identifier><identifier>DOI: 10.3892/etm.2021.11039</identifier><identifier>PMID: 34970339</identifier><language>eng</language><publisher>Greece: Spandidos Publications</publisher><subject>Abdomen ; Alcohol ; Antibodies ; Care and treatment ; Cellular signal transduction ; Chemical properties ; Coronary vessels ; Development and progression ; Fibrosis ; Glioma ; Growth factors ; Health aspects ; Laboratory animals ; Liver cancer ; Liver diseases ; Medical research ; Membranes ; Physiological aspects ; Phytochemicals ; Proteins ; Salvia ; Science</subject><ispartof>Experimental and therapeutic medicine, 2022-02, Vol.23 (2), p.116, Article 116</ispartof><rights>Copyright: © Tao et al.</rights><rights>COPYRIGHT 2022 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2022</rights><rights>Copyright: © Tao et al. 2020</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c415t-4e8e4ff0f8d3b5818c1e7cba80afe93b29e3f48e20d83b1695541cae12601d293</citedby><cites>FETCH-LOGICAL-c415t-4e8e4ff0f8d3b5818c1e7cba80afe93b29e3f48e20d83b1695541cae12601d293</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8713182/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8713182/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34970339$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tao, Shanjun</creatorcontrib><creatorcontrib>Duan, Renjie</creatorcontrib><creatorcontrib>Xu, Tong</creatorcontrib><creatorcontrib>Hong, Jiao</creatorcontrib><creatorcontrib>Gu, Wenjie</creatorcontrib><creatorcontrib>Lin, Aiqin</creatorcontrib><creatorcontrib>Lian, Likai</creatorcontrib><creatorcontrib>Huang, Haoyu</creatorcontrib><creatorcontrib>Lu, Jiangtao</creatorcontrib><creatorcontrib>Li, Tiechen</creatorcontrib><title>Salvianolic acid B inhibits the progression of liver fibrosis in rats via modulation of the Hedgehog signaling pathway</title><title>Experimental and therapeutic medicine</title><addtitle>Exp Ther Med</addtitle><description>Salvianolic acid B (Sal B) has previously reported anti-hepatic fibrosis effects, though it is not clear if it can inhibit hepatic fibrosis by regulating the hedgehog (Hh) signaling pathway. The aim of the present study was to explore the roles and mechanism of Sal B in preventing and treating liver fibrosis in rats. The study also aimed to determine the role of the Hh signaling pathway in this process. A rat model of liver fibrosis was induced through the subcutaneous injection of 50% carbon tetrachloride, followed by treatment with Sal B. After gavage, blood was collected to detect serum markers of liver injury. The degree of liver fibrosis and tissue damage was assessed using histopathological analysis. Western blotting and reverse transcription-quantitative PCR were used to detect the expression levels of TGF-β1 and Hh signaling pathway-related genes, including Sonic hedgehog (Shh) protein, membrane protein receptor protein patched homolog 1 (Ptch1), membrane protein receptor Smoothened (Smo) and transcription factor glioma-associated oncogene homolog 1 (Gli1). Serum alanine aminotransferase, aspartate aminotransferase and total bilirubin levels were decreased, whilst levels of albumin were increased in rats with liver fibrosis that were treated with Sal B (P<0.05). Additionally, significant increases in TGF-β1, Shh, Ptch1, Smo, Gli1 and α-smooth muscle actin expression levels were observed in the liver tissues of rats with hepatic fibrosis (P<0.05). However, Sal B treatment significantly reduced the expression levels of these proteins (P<0.05). In conclusion, the results of the present study suggested that the Hh signaling pathway may be activated during the process of rat liver fibrosis. Thus, Sal B may exert its anti-hepatic fibrosis effects, at least in part, by inhibiting the activation of the Hh signaling pathway.</description><subject>Abdomen</subject><subject>Alcohol</subject><subject>Antibodies</subject><subject>Care and treatment</subject><subject>Cellular signal transduction</subject><subject>Chemical properties</subject><subject>Coronary vessels</subject><subject>Development and progression</subject><subject>Fibrosis</subject><subject>Glioma</subject><subject>Growth factors</subject><subject>Health aspects</subject><subject>Laboratory animals</subject><subject>Liver cancer</subject><subject>Liver diseases</subject><subject>Medical research</subject><subject>Membranes</subject><subject>Physiological aspects</subject><subject>Phytochemicals</subject><subject>Proteins</subject><subject>Salvia</subject><subject>Science</subject><issn>1792-0981</issn><issn>1792-1015</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>BENPR</sourceid><recordid>eNptksFvFCEUxomxsU3bq0dD4nlXHszswMWkNmpNmnhoPROGecy8ZmZYYXZN_3tZXasmhQMEft-X9-Bj7DWItdJGvsNlWkshYQ0glHnBzqAxcgUC6pfHvTAaTtllzg-ijHoDWtev2KmqTCOUMmdsf-fGPbk5juS589TxD5zmgVpaMl8G5NsU-4Q5U5x5DHykPSYeqE0xUy4oT66QxYJPsduNbjmCB-0Ndj0OseeZ-tmNNPd865bhh3u8YCfBjRkvj-s5-_bp4_31zer26-cv11e3K19Bvawq1FiFIILuVFtr0B6w8a3TwgU0qpUGVag0StFp1cLG1HUF3iHIjYBOGnXO3v_23e7aCTuP85LcaLeJJpcebXRk_7-ZabB93FvdgAIti8Hbo0GK33eYF_sQd6k0k63cSKVVo6rmL9W7ES3NIRYzP1H29qoUpeqq0VCo9TNUmR1O5OOMgcr5cwJfXjsnDE-Fg7CHBNiSAHtIgP2VgCJ482-7T_if_1Y_AROtrVo</recordid><startdate>20220201</startdate><enddate>20220201</enddate><creator>Tao, Shanjun</creator><creator>Duan, Renjie</creator><creator>Xu, Tong</creator><creator>Hong, Jiao</creator><creator>Gu, Wenjie</creator><creator>Lin, Aiqin</creator><creator>Lian, Likai</creator><creator>Huang, Haoyu</creator><creator>Lu, Jiangtao</creator><creator>Li, Tiechen</creator><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</general><general>D.A. 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The aim of the present study was to explore the roles and mechanism of Sal B in preventing and treating liver fibrosis in rats. The study also aimed to determine the role of the Hh signaling pathway in this process. A rat model of liver fibrosis was induced through the subcutaneous injection of 50% carbon tetrachloride, followed by treatment with Sal B. After gavage, blood was collected to detect serum markers of liver injury. The degree of liver fibrosis and tissue damage was assessed using histopathological analysis. Western blotting and reverse transcription-quantitative PCR were used to detect the expression levels of TGF-β1 and Hh signaling pathway-related genes, including Sonic hedgehog (Shh) protein, membrane protein receptor protein patched homolog 1 (Ptch1), membrane protein receptor Smoothened (Smo) and transcription factor glioma-associated oncogene homolog 1 (Gli1). Serum alanine aminotransferase, aspartate aminotransferase and total bilirubin levels were decreased, whilst levels of albumin were increased in rats with liver fibrosis that were treated with Sal B (P<0.05). Additionally, significant increases in TGF-β1, Shh, Ptch1, Smo, Gli1 and α-smooth muscle actin expression levels were observed in the liver tissues of rats with hepatic fibrosis (P<0.05). However, Sal B treatment significantly reduced the expression levels of these proteins (P<0.05). In conclusion, the results of the present study suggested that the Hh signaling pathway may be activated during the process of rat liver fibrosis. Thus, Sal B may exert its anti-hepatic fibrosis effects, at least in part, by inhibiting the activation of the Hh signaling pathway.</abstract><cop>Greece</cop><pub>Spandidos Publications</pub><pmid>34970339</pmid><doi>10.3892/etm.2021.11039</doi><oa>free_for_read</oa></addata></record> |
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| subjects | Abdomen Alcohol Antibodies Care and treatment Cellular signal transduction Chemical properties Coronary vessels Development and progression Fibrosis Glioma Growth factors Health aspects Laboratory animals Liver cancer Liver diseases Medical research Membranes Physiological aspects Phytochemicals Proteins Salvia Science |
| title | Salvianolic acid B inhibits the progression of liver fibrosis in rats via modulation of the Hedgehog signaling pathway |
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