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Preventive and therapeutic effects of angiotensin II type 1 receptor blocker on hepatic fibrosis induced by bile duct ligation in rats
The aim of this study was to examine the preventive and therapeutic effects of an angiotensin II type 1 receptor blocker, candesartan, on cholestasis-induced liver fibrosis. Candesartan was administered orally for 21 days immediately after bile duct ligation to evaluate its preventive effect, and fo...
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| Published in: | Journal of gastroenterology 2006-10, Vol.41 (10), p.996-1004 |
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| creator | Ueki, Masaru Koda, Masahiko Yamamoto, Satoru Matsunaga, Yoshiko Murawaki, Yoshikazu |
| description | The aim of this study was to examine the preventive and therapeutic effects of an angiotensin II type 1 receptor blocker, candesartan, on cholestasis-induced liver fibrosis.
Candesartan was administered orally for 21 days immediately after bile duct ligation to evaluate its preventive effect, and for 21 days starting 3 weeks after bile duct ligation to evaluate its therapeutic effect. Fibrosis was assessed by measuring hepatic hydroxyproline (Hyp) content. The activated hepatic stellate cells (HSCs) were assessed by alpha-smooth muscle actin (alpha-SMA) immunostaining. The gene expression of collagen I, transforming growth factor-beta1 (TGF-beta1), and connective tissue growth factor (CTGF) in the liver was examined by real-time reverse transcriptase-polymerase chain reaction.
As a preventive effect, candesartan reduced the hepatic Hyp content by 36%, alpha-SMA-positive cells by 65%, hepatic TGF-beta1 content by 35%, and the expression of collagen I by 72%, TGF-beta1 by 67%, and CTGF mRNA by 69%. As a therapeutic effect, candesartan reduced the hepatic Hyp content by 48%, TGF-beta1 content by 54%, and the expression of collagen I by 47%, TGF-beta1 by 43%, and CTGF mRNA by 53%. Significant decreases in lipid peroxidation markers, hepatic thiobarbituric acid-reactive substance, and 4-hydroxy-2-nonenal were observed in candesartan-treated rats.
Candesartan attenuated liver fibrosis via suppression of collagen I and TGF-beta1 expression, HSC activation, and lipid peroxidation protein, showing its preventive and therapeutic effects on cholestasis-induced liver fibrosis. |
| doi_str_mv | 10.1007/s00535-006-1891-1 |
| format | article |
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Candesartan was administered orally for 21 days immediately after bile duct ligation to evaluate its preventive effect, and for 21 days starting 3 weeks after bile duct ligation to evaluate its therapeutic effect. Fibrosis was assessed by measuring hepatic hydroxyproline (Hyp) content. The activated hepatic stellate cells (HSCs) were assessed by alpha-smooth muscle actin (alpha-SMA) immunostaining. The gene expression of collagen I, transforming growth factor-beta1 (TGF-beta1), and connective tissue growth factor (CTGF) in the liver was examined by real-time reverse transcriptase-polymerase chain reaction.
As a preventive effect, candesartan reduced the hepatic Hyp content by 36%, alpha-SMA-positive cells by 65%, hepatic TGF-beta1 content by 35%, and the expression of collagen I by 72%, TGF-beta1 by 67%, and CTGF mRNA by 69%. As a therapeutic effect, candesartan reduced the hepatic Hyp content by 48%, TGF-beta1 content by 54%, and the expression of collagen I by 47%, TGF-beta1 by 43%, and CTGF mRNA by 53%. Significant decreases in lipid peroxidation markers, hepatic thiobarbituric acid-reactive substance, and 4-hydroxy-2-nonenal were observed in candesartan-treated rats.
Candesartan attenuated liver fibrosis via suppression of collagen I and TGF-beta1 expression, HSC activation, and lipid peroxidation protein, showing its preventive and therapeutic effects on cholestasis-induced liver fibrosis.</description><identifier>ISSN: 0944-1174</identifier><identifier>EISSN: 1435-5922</identifier><identifier>DOI: 10.1007/s00535-006-1891-1</identifier><identifier>PMID: 17096069</identifier><language>eng</language><publisher>Japan: Springer Nature B.V</publisher><subject>Actin ; Angiotensin ; Angiotensin II ; Angiotensin II Type 1 Receptor Blockers - therapeutic use ; Animals ; Benzimidazoles - therapeutic use ; Bile ducts ; Biphenyl Compounds ; Cells, Cultured ; Cholestasis ; Collagen ; Collagen (type I) ; Common Bile Duct - surgery ; Connective Tissue Growth Factor ; Connective tissues ; Enzyme-Linked Immunosorbent Assay ; Fibrosis ; Follow-Up Studies ; Gallbladder diseases ; Gene Expression ; Growth factors ; Hydroxyproline ; Hydroxyproline - metabolism ; Immediate-Early Proteins - genetics ; Immediate-Early Proteins - metabolism ; Insulin-Like Growth Factor Binding Proteins ; Intercellular Signaling Peptides and Proteins - genetics ; Intercellular Signaling Peptides and Proteins - metabolism ; Ligation ; Lipid peroxidation ; Liver ; Liver - metabolism ; Liver - pathology ; Liver Cirrhosis, Experimental - etiology ; Liver Cirrhosis, Experimental - metabolism ; Liver Cirrhosis, Experimental - prevention & control ; Male ; Oral administration ; Polymerase Chain Reaction ; Rats ; Rats, Wistar ; RNA - genetics ; RNA-directed DNA polymerase ; Smooth muscle ; Stellate cells ; Tetrazoles - therapeutic use ; Thiobarbituric acid ; Transforming Growth Factor beta1 - genetics ; Transforming Growth Factor beta1 - metabolism ; Transforming growth factor-b1 ; Treatment Outcome</subject><ispartof>Journal of gastroenterology, 2006-10, Vol.41 (10), p.996-1004</ispartof><rights>Springer-Verlag Tokyo 2006</rights><rights>Springer-Verlag Tokyo 2006.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c444t-1445e1fd3b79a50a1ce1f542239c4927317c1a9561d4155ff2f6f35273a454993</citedby><cites>FETCH-LOGICAL-c444t-1445e1fd3b79a50a1ce1f542239c4927317c1a9561d4155ff2f6f35273a454993</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27922,27923</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17096069$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ueki, Masaru</creatorcontrib><creatorcontrib>Koda, Masahiko</creatorcontrib><creatorcontrib>Yamamoto, Satoru</creatorcontrib><creatorcontrib>Matsunaga, Yoshiko</creatorcontrib><creatorcontrib>Murawaki, Yoshikazu</creatorcontrib><title>Preventive and therapeutic effects of angiotensin II type 1 receptor blocker on hepatic fibrosis induced by bile duct ligation in rats</title><title>Journal of gastroenterology</title><addtitle>J Gastroenterol</addtitle><description>The aim of this study was to examine the preventive and therapeutic effects of an angiotensin II type 1 receptor blocker, candesartan, on cholestasis-induced liver fibrosis.
Candesartan was administered orally for 21 days immediately after bile duct ligation to evaluate its preventive effect, and for 21 days starting 3 weeks after bile duct ligation to evaluate its therapeutic effect. Fibrosis was assessed by measuring hepatic hydroxyproline (Hyp) content. The activated hepatic stellate cells (HSCs) were assessed by alpha-smooth muscle actin (alpha-SMA) immunostaining. The gene expression of collagen I, transforming growth factor-beta1 (TGF-beta1), and connective tissue growth factor (CTGF) in the liver was examined by real-time reverse transcriptase-polymerase chain reaction.
As a preventive effect, candesartan reduced the hepatic Hyp content by 36%, alpha-SMA-positive cells by 65%, hepatic TGF-beta1 content by 35%, and the expression of collagen I by 72%, TGF-beta1 by 67%, and CTGF mRNA by 69%. As a therapeutic effect, candesartan reduced the hepatic Hyp content by 48%, TGF-beta1 content by 54%, and the expression of collagen I by 47%, TGF-beta1 by 43%, and CTGF mRNA by 53%. Significant decreases in lipid peroxidation markers, hepatic thiobarbituric acid-reactive substance, and 4-hydroxy-2-nonenal were observed in candesartan-treated rats.
Candesartan attenuated liver fibrosis via suppression of collagen I and TGF-beta1 expression, HSC activation, and lipid peroxidation protein, showing its preventive and therapeutic effects on cholestasis-induced liver fibrosis.</description><subject>Actin</subject><subject>Angiotensin</subject><subject>Angiotensin II</subject><subject>Angiotensin II Type 1 Receptor Blockers - therapeutic use</subject><subject>Animals</subject><subject>Benzimidazoles - therapeutic use</subject><subject>Bile ducts</subject><subject>Biphenyl Compounds</subject><subject>Cells, Cultured</subject><subject>Cholestasis</subject><subject>Collagen</subject><subject>Collagen (type I)</subject><subject>Common Bile Duct - surgery</subject><subject>Connective Tissue Growth Factor</subject><subject>Connective tissues</subject><subject>Enzyme-Linked Immunosorbent Assay</subject><subject>Fibrosis</subject><subject>Follow-Up Studies</subject><subject>Gallbladder diseases</subject><subject>Gene Expression</subject><subject>Growth factors</subject><subject>Hydroxyproline</subject><subject>Hydroxyproline - metabolism</subject><subject>Immediate-Early Proteins - genetics</subject><subject>Immediate-Early Proteins - metabolism</subject><subject>Insulin-Like Growth Factor Binding Proteins</subject><subject>Intercellular Signaling Peptides and Proteins - genetics</subject><subject>Intercellular Signaling Peptides and Proteins - metabolism</subject><subject>Ligation</subject><subject>Lipid peroxidation</subject><subject>Liver</subject><subject>Liver - metabolism</subject><subject>Liver - pathology</subject><subject>Liver Cirrhosis, Experimental - etiology</subject><subject>Liver Cirrhosis, Experimental - metabolism</subject><subject>Liver Cirrhosis, Experimental - prevention & control</subject><subject>Male</subject><subject>Oral administration</subject><subject>Polymerase Chain Reaction</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>RNA - genetics</subject><subject>RNA-directed DNA polymerase</subject><subject>Smooth muscle</subject><subject>Stellate cells</subject><subject>Tetrazoles - therapeutic use</subject><subject>Thiobarbituric acid</subject><subject>Transforming Growth Factor beta1 - genetics</subject><subject>Transforming Growth Factor beta1 - metabolism</subject><subject>Transforming growth factor-b1</subject><subject>Treatment Outcome</subject><issn>0944-1174</issn><issn>1435-5922</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><recordid>eNp1kd9qFDEUh4Modlt9AG8kKPRuNGfyZzaXUmxdKOhFvQ6ZzEmbOjsZk0xhX8DnboZdEASvwsn5zpdwfoS8A_YJGOs-Z8Yklw1jqoGthgZekA2IeiN1274kG6aFaAA6cUbOc35kDDiT29fkDDqmFVN6Q_78SPiEUwlPSO000PKAyc64lOAoeo-uZBp9bd2HWHDKYaK7HS2HGSnQhA7nEhPtx-h-YaJxog8423XYhz7FHDIN07A4HGh_oH0Ykdaq0DHcV6ri1ZdsyW_IK2_HjG9P5wX5ef317upbc_v9Znf15bZxQojSgBASwQ-877SVzIKrlRRty7UTuu04dA6slgoGAVJ633rluawNK6TQml-Qy6N3TvH3grmYfcgOx9FOGJds1HZdUccr-PEf8DEuaap_M61SAnR9Cyr14b8UdFA9WlUIjpCrC8kJvZlT2Nt0MMDMmqM55mhqjmbN0azi9yfx0u9x-DtxCo4_A2qFl6s</recordid><startdate>200610</startdate><enddate>200610</enddate><creator>Ueki, Masaru</creator><creator>Koda, Masahiko</creator><creator>Yamamoto, Satoru</creator><creator>Matsunaga, Yoshiko</creator><creator>Murawaki, Yoshikazu</creator><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7RV</scope><scope>7T5</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9-</scope><scope>K9.</scope><scope>KB0</scope><scope>M0R</scope><scope>M0S</scope><scope>M1P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>8BM</scope></search><sort><creationdate>200610</creationdate><title>Preventive and therapeutic effects of angiotensin II type 1 receptor blocker on hepatic fibrosis induced by bile duct ligation in rats</title><author>Ueki, Masaru ; Koda, Masahiko ; Yamamoto, Satoru ; Matsunaga, Yoshiko ; Murawaki, Yoshikazu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c444t-1445e1fd3b79a50a1ce1f542239c4927317c1a9561d4155ff2f6f35273a454993</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Actin</topic><topic>Angiotensin</topic><topic>Angiotensin II</topic><topic>Angiotensin II Type 1 Receptor Blockers - therapeutic use</topic><topic>Animals</topic><topic>Benzimidazoles - therapeutic use</topic><topic>Bile ducts</topic><topic>Biphenyl Compounds</topic><topic>Cells, Cultured</topic><topic>Cholestasis</topic><topic>Collagen</topic><topic>Collagen (type I)</topic><topic>Common Bile Duct - surgery</topic><topic>Connective Tissue Growth Factor</topic><topic>Connective tissues</topic><topic>Enzyme-Linked Immunosorbent Assay</topic><topic>Fibrosis</topic><topic>Follow-Up Studies</topic><topic>Gallbladder diseases</topic><topic>Gene Expression</topic><topic>Growth factors</topic><topic>Hydroxyproline</topic><topic>Hydroxyproline - metabolism</topic><topic>Immediate-Early Proteins - genetics</topic><topic>Immediate-Early Proteins - metabolism</topic><topic>Insulin-Like Growth Factor Binding Proteins</topic><topic>Intercellular Signaling Peptides and Proteins - genetics</topic><topic>Intercellular Signaling Peptides and Proteins - metabolism</topic><topic>Ligation</topic><topic>Lipid peroxidation</topic><topic>Liver</topic><topic>Liver - 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Academic</collection><collection>ComDisDome</collection><jtitle>Journal of gastroenterology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ueki, Masaru</au><au>Koda, Masahiko</au><au>Yamamoto, Satoru</au><au>Matsunaga, Yoshiko</au><au>Murawaki, Yoshikazu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Preventive and therapeutic effects of angiotensin II type 1 receptor blocker on hepatic fibrosis induced by bile duct ligation in rats</atitle><jtitle>Journal of gastroenterology</jtitle><addtitle>J Gastroenterol</addtitle><date>2006-10</date><risdate>2006</risdate><volume>41</volume><issue>10</issue><spage>996</spage><epage>1004</epage><pages>996-1004</pages><issn>0944-1174</issn><eissn>1435-5922</eissn><abstract>The aim of this study was to examine the preventive and therapeutic effects of an angiotensin II type 1 receptor blocker, candesartan, on cholestasis-induced liver fibrosis.
Candesartan was administered orally for 21 days immediately after bile duct ligation to evaluate its preventive effect, and for 21 days starting 3 weeks after bile duct ligation to evaluate its therapeutic effect. Fibrosis was assessed by measuring hepatic hydroxyproline (Hyp) content. The activated hepatic stellate cells (HSCs) were assessed by alpha-smooth muscle actin (alpha-SMA) immunostaining. The gene expression of collagen I, transforming growth factor-beta1 (TGF-beta1), and connective tissue growth factor (CTGF) in the liver was examined by real-time reverse transcriptase-polymerase chain reaction.
As a preventive effect, candesartan reduced the hepatic Hyp content by 36%, alpha-SMA-positive cells by 65%, hepatic TGF-beta1 content by 35%, and the expression of collagen I by 72%, TGF-beta1 by 67%, and CTGF mRNA by 69%. As a therapeutic effect, candesartan reduced the hepatic Hyp content by 48%, TGF-beta1 content by 54%, and the expression of collagen I by 47%, TGF-beta1 by 43%, and CTGF mRNA by 53%. Significant decreases in lipid peroxidation markers, hepatic thiobarbituric acid-reactive substance, and 4-hydroxy-2-nonenal were observed in candesartan-treated rats.
Candesartan attenuated liver fibrosis via suppression of collagen I and TGF-beta1 expression, HSC activation, and lipid peroxidation protein, showing its preventive and therapeutic effects on cholestasis-induced liver fibrosis.</abstract><cop>Japan</cop><pub>Springer Nature B.V</pub><pmid>17096069</pmid><doi>10.1007/s00535-006-1891-1</doi><tpages>9</tpages></addata></record> |
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| subjects | Actin Angiotensin Angiotensin II Angiotensin II Type 1 Receptor Blockers - therapeutic use Animals Benzimidazoles - therapeutic use Bile ducts Biphenyl Compounds Cells, Cultured Cholestasis Collagen Collagen (type I) Common Bile Duct - surgery Connective Tissue Growth Factor Connective tissues Enzyme-Linked Immunosorbent Assay Fibrosis Follow-Up Studies Gallbladder diseases Gene Expression Growth factors Hydroxyproline Hydroxyproline - metabolism Immediate-Early Proteins - genetics Immediate-Early Proteins - metabolism Insulin-Like Growth Factor Binding Proteins Intercellular Signaling Peptides and Proteins - genetics Intercellular Signaling Peptides and Proteins - metabolism Ligation Lipid peroxidation Liver Liver - metabolism Liver - pathology Liver Cirrhosis, Experimental - etiology Liver Cirrhosis, Experimental - metabolism Liver Cirrhosis, Experimental - prevention & control Male Oral administration Polymerase Chain Reaction Rats Rats, Wistar RNA - genetics RNA-directed DNA polymerase Smooth muscle Stellate cells Tetrazoles - therapeutic use Thiobarbituric acid Transforming Growth Factor beta1 - genetics Transforming Growth Factor beta1 - metabolism Transforming growth factor-b1 Treatment Outcome |
| title | Preventive and therapeutic effects of angiotensin II type 1 receptor blocker on hepatic fibrosis induced by bile duct ligation in rats |
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