Protective effects of S-adenosylmethionine against CCl4- and ethanol-induced experimental hepatic fibrosis
In this study the effects of S-adenosylmethionine (SAM) on experimental hepatic fibrotic rats induced by carbon tetrachloride (CCl 4 ) and ethanol and the relevant potential mechanisms were explored. Hepatic fibrotic rat models were established with CCl 4 diluted in olive oil being drunk with 10% et...
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Veröffentlicht in: | Molecular biology (New York) 2016-03, Vol.50 (2), p.246-251 |
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creator | Zhang, F. Gu, J.-X. Zou, X.-P. Zhuge, Y.-Z. |
description | In this study the effects of S-adenosylmethionine (SAM) on experimental hepatic fibrotic rats induced by carbon tetrachloride (CCl
4
) and ethanol and the relevant potential mechanisms were explored. Hepatic fibrotic rat models were established with CCl
4
diluted in olive oil being drunk with 10% ethanol in water. SAM was used both for prevention and treatment. Histological evaluation was carried out by hematoxylin- eosin (HE) and Masson staining of hepatic samples. Serum biochemical assays showed that alanine aminotransferase (ALT) was increased and albumin (ALB) was decreased by CCl
4
and ethanol, and both effects were suppressed by preventing and treating use of SAM. The model control rats got significantly higher scores in fatty degeneration, lobular inflammation, and hepatocyte ballooning. A significant improvement was observed in the SAM-prevented rats and SAM-treated rats, which was consistent with the change of fibrosis scoring in each group. Smad3 was induced by CCl
4
and ethanol in the model control group, which was significantly down regulated by SAM. SAM reduced both total Smad3 and phospho-Smad3 in vitro. SAM had a protective effect on hepatic fibrosis in rats induced by CCl
4
combined with ethanol and the down-regulation of activity and expression of Smad3 were involved in the potential mechanisms. |
doi_str_mv | 10.1134/S0026893316020278 |
format | Article |
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4
) and ethanol and the relevant potential mechanisms were explored. Hepatic fibrotic rat models were established with CCl
4
diluted in olive oil being drunk with 10% ethanol in water. SAM was used both for prevention and treatment. Histological evaluation was carried out by hematoxylin- eosin (HE) and Masson staining of hepatic samples. Serum biochemical assays showed that alanine aminotransferase (ALT) was increased and albumin (ALB) was decreased by CCl
4
and ethanol, and both effects were suppressed by preventing and treating use of SAM. The model control rats got significantly higher scores in fatty degeneration, lobular inflammation, and hepatocyte ballooning. A significant improvement was observed in the SAM-prevented rats and SAM-treated rats, which was consistent with the change of fibrosis scoring in each group. Smad3 was induced by CCl
4
and ethanol in the model control group, which was significantly down regulated by SAM. SAM reduced both total Smad3 and phospho-Smad3 in vitro. SAM had a protective effect on hepatic fibrosis in rats induced by CCl
4
combined with ethanol and the down-regulation of activity and expression of Smad3 were involved in the potential mechanisms.</description><identifier>ISSN: 0026-8933</identifier><identifier>EISSN: 1608-3245</identifier><identifier>DOI: 10.1134/S0026893316020278</identifier><language>eng</language><publisher>Moscow: Pleiades Publishing</publisher><subject>Biochemistry ; Biomedical and Life Sciences ; Ethanol ; Histology ; Human Genetics ; Life Sciences ; Liver ; Molecular biology ; Molecular Cell Biology</subject><ispartof>Molecular biology (New York), 2016-03, Vol.50 (2), p.246-251</ispartof><rights>Pleiades Publishing, Inc. 2016</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c316t-64e6c2bcff374127e53c3055f56cde2a3746f6973d7548f18f81d85e2293c083</citedby><cites>FETCH-LOGICAL-c316t-64e6c2bcff374127e53c3055f56cde2a3746f6973d7548f18f81d85e2293c083</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1134/S0026893316020278$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1134/S0026893316020278$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27903,27904,41467,42536,51298</link.rule.ids></links><search><creatorcontrib>Zhang, F.</creatorcontrib><creatorcontrib>Gu, J.-X.</creatorcontrib><creatorcontrib>Zou, X.-P.</creatorcontrib><creatorcontrib>Zhuge, Y.-Z.</creatorcontrib><title>Protective effects of S-adenosylmethionine against CCl4- and ethanol-induced experimental hepatic fibrosis</title><title>Molecular biology (New York)</title><addtitle>Mol Biol</addtitle><description>In this study the effects of S-adenosylmethionine (SAM) on experimental hepatic fibrotic rats induced by carbon tetrachloride (CCl
4
) and ethanol and the relevant potential mechanisms were explored. Hepatic fibrotic rat models were established with CCl
4
diluted in olive oil being drunk with 10% ethanol in water. SAM was used both for prevention and treatment. Histological evaluation was carried out by hematoxylin- eosin (HE) and Masson staining of hepatic samples. Serum biochemical assays showed that alanine aminotransferase (ALT) was increased and albumin (ALB) was decreased by CCl
4
and ethanol, and both effects were suppressed by preventing and treating use of SAM. The model control rats got significantly higher scores in fatty degeneration, lobular inflammation, and hepatocyte ballooning. A significant improvement was observed in the SAM-prevented rats and SAM-treated rats, which was consistent with the change of fibrosis scoring in each group. Smad3 was induced by CCl
4
and ethanol in the model control group, which was significantly down regulated by SAM. SAM reduced both total Smad3 and phospho-Smad3 in vitro. SAM had a protective effect on hepatic fibrosis in rats induced by CCl
4
combined with ethanol and the down-regulation of activity and expression of Smad3 were involved in the potential mechanisms.</description><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Ethanol</subject><subject>Histology</subject><subject>Human Genetics</subject><subject>Life Sciences</subject><subject>Liver</subject><subject>Molecular biology</subject><subject>Molecular Cell Biology</subject><issn>0026-8933</issn><issn>1608-3245</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp1UEtLAzEQDqJgrf4AbwHP0Tz2kT3KolYoKLT3Jc1O2pRtsiap2H9vSj0IIgQyk-8xXwahW0bvGRPFw4JSXslGCFZRTnktz9Akl5IIXpTnaHKEyRG_RFcxbill-fAJ2r4Hn0An-wkYjMlVxN7gBVE9OB8Pww7SxnpnHWC1VtbFhNt2KAhWrscZU84PxLp-ryH3XyMEuwOX1IA3MKpkNTZ2FXy08RpdGDVEuPm5p2j5_LRsZ2T-9vLaPs6JzuETqQqoNF9pY0RdMF5DKbSgZWnKSvfAVX6tTNXUoq_LQhomjWS9LIHzRmgqxRTdnWzH4D_2EFO39fvg8sSO1bJu8s8bmlnsxNI5WwxgujEHV-HQMdodN9r92WjW8JMmZq5bQ_jl_K_oGyoCeBY</recordid><startdate>20160301</startdate><enddate>20160301</enddate><creator>Zhang, F.</creator><creator>Gu, J.-X.</creator><creator>Zou, X.-P.</creator><creator>Zhuge, Y.-Z.</creator><general>Pleiades Publishing</general><general>Springer Nature B.V</general><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>RC3</scope></search><sort><creationdate>20160301</creationdate><title>Protective effects of S-adenosylmethionine against CCl4- and ethanol-induced experimental hepatic fibrosis</title><author>Zhang, F. ; Gu, J.-X. ; Zou, X.-P. ; Zhuge, Y.-Z.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c316t-64e6c2bcff374127e53c3055f56cde2a3746f6973d7548f18f81d85e2293c083</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Ethanol</topic><topic>Histology</topic><topic>Human Genetics</topic><topic>Life Sciences</topic><topic>Liver</topic><topic>Molecular biology</topic><topic>Molecular Cell Biology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhang, F.</creatorcontrib><creatorcontrib>Gu, J.-X.</creatorcontrib><creatorcontrib>Zou, X.-P.</creatorcontrib><creatorcontrib>Zhuge, Y.-Z.</creatorcontrib><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><jtitle>Molecular biology (New York)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, F.</au><au>Gu, J.-X.</au><au>Zou, X.-P.</au><au>Zhuge, Y.-Z.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Protective effects of S-adenosylmethionine against CCl4- and ethanol-induced experimental hepatic fibrosis</atitle><jtitle>Molecular biology (New York)</jtitle><stitle>Mol Biol</stitle><date>2016-03-01</date><risdate>2016</risdate><volume>50</volume><issue>2</issue><spage>246</spage><epage>251</epage><pages>246-251</pages><issn>0026-8933</issn><eissn>1608-3245</eissn><abstract>In this study the effects of S-adenosylmethionine (SAM) on experimental hepatic fibrotic rats induced by carbon tetrachloride (CCl
4
) and ethanol and the relevant potential mechanisms were explored. Hepatic fibrotic rat models were established with CCl
4
diluted in olive oil being drunk with 10% ethanol in water. SAM was used both for prevention and treatment. Histological evaluation was carried out by hematoxylin- eosin (HE) and Masson staining of hepatic samples. Serum biochemical assays showed that alanine aminotransferase (ALT) was increased and albumin (ALB) was decreased by CCl
4
and ethanol, and both effects were suppressed by preventing and treating use of SAM. The model control rats got significantly higher scores in fatty degeneration, lobular inflammation, and hepatocyte ballooning. A significant improvement was observed in the SAM-prevented rats and SAM-treated rats, which was consistent with the change of fibrosis scoring in each group. Smad3 was induced by CCl
4
and ethanol in the model control group, which was significantly down regulated by SAM. SAM reduced both total Smad3 and phospho-Smad3 in vitro. SAM had a protective effect on hepatic fibrosis in rats induced by CCl
4
combined with ethanol and the down-regulation of activity and expression of Smad3 were involved in the potential mechanisms.</abstract><cop>Moscow</cop><pub>Pleiades Publishing</pub><doi>10.1134/S0026893316020278</doi><tpages>6</tpages></addata></record> |
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subjects | Biochemistry Biomedical and Life Sciences Ethanol Histology Human Genetics Life Sciences Liver Molecular biology Molecular Cell Biology |
title | Protective effects of S-adenosylmethionine against CCl4- and ethanol-induced experimental hepatic fibrosis |
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