Angiotensin II type 1 receptor blocker inhibits fibrosis in rat nonalcoholic steatohepatitis
Nonalcoholic steatohepatitis (NASH) is now the most frequent cause of chronic liver impairment in developed countries and is a suggested causative factor in the development of cryptogenic cirrhosis and hepatocellular carcinoma. At present there is no effective and accepted therapy for NASH. The reni...
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| Veröffentlicht in: | Hepatology (Baltimore, Md.) Md.), 2007-06, Vol.45 (6), p.1375-1381 |
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| creator | Hirose, Akira Ono, Masafumi Saibara, Toshiji Nozaki, Yasuko Masuda, Kosei Yoshioka, Akemi Takahashi, Masaya Akisawa, Naoaki Iwasaki, Shinji Oben, Jude A. Onishi, Saburo |
| description | Nonalcoholic steatohepatitis (NASH) is now the most frequent cause of chronic liver impairment in developed countries and is a suggested causative factor in the development of cryptogenic cirrhosis and hepatocellular carcinoma. At present there is no effective and accepted therapy for NASH. The renin‐angiotensin system is involved in hepatic fibrosis through activation of hepatic stellate cells, major fibrogenic cells in the liver. Hepatic stellate cells are activated by liver injury to express excessive matrix proteins and profibrogenic cytokines such as transforming growth factor–beta 1. Medicines that inhibit this pathway may be of therapeutic potential in NASH. Using a methionine‐choline–deficient rat model of NASH, we studied the potential utility of an angiotensin II type 1 receptor blocker (ARB), olmesartan, on biochemical, histologic, and antioxidant measures of disease activity. ARB significantly attenuated increases in aspartate aminotransferase, activation of hepatic stellate cells, oxidative stress, expression of transforming growth factor–beta 1, expression of collagen genes, and liver fibrosis. Conclusion: Our observations strongly suggest a potential preventive role for ARB in the progression of nonalcoholic steatohepatitis. (HEPATOLOGY 2007.) |
| doi_str_mv | 10.1002/hep.21638 |
| format | Article |
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At present there is no effective and accepted therapy for NASH. The renin‐angiotensin system is involved in hepatic fibrosis through activation of hepatic stellate cells, major fibrogenic cells in the liver. Hepatic stellate cells are activated by liver injury to express excessive matrix proteins and profibrogenic cytokines such as transforming growth factor–beta 1. Medicines that inhibit this pathway may be of therapeutic potential in NASH. Using a methionine‐choline–deficient rat model of NASH, we studied the potential utility of an angiotensin II type 1 receptor blocker (ARB), olmesartan, on biochemical, histologic, and antioxidant measures of disease activity. ARB significantly attenuated increases in aspartate aminotransferase, activation of hepatic stellate cells, oxidative stress, expression of transforming growth factor–beta 1, expression of collagen genes, and liver fibrosis. Conclusion: Our observations strongly suggest a potential preventive role for ARB in the progression of nonalcoholic steatohepatitis. (HEPATOLOGY 2007.)</description><identifier>ISSN: 0270-9139</identifier><identifier>EISSN: 1527-3350</identifier><identifier>DOI: 10.1002/hep.21638</identifier><identifier>PMID: 17518368</identifier><identifier>CODEN: HPTLD9</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>Angiotensin II Type 1 Receptor Blockers - pharmacology ; Animal Feed ; Animals ; Antibiotics. Antiinfectious agents. Antiparasitic agents ; Antiseptics ; Biological and medical sciences ; Choline - pharmacology ; Connective Tissue Growth Factor ; Fatty Liver - drug therapy ; Fatty Liver - pathology ; Gastroenterology. Liver. Pancreas. Abdomen ; Imidazoles - pharmacology ; Immediate-Early Proteins - metabolism ; Intercellular Signaling Peptides and Proteins - metabolism ; Liver Cirrhosis - drug therapy ; Liver Cirrhosis - pathology ; Liver Cirrhosis - prevention & control ; Liver. Biliary tract. Portal circulation. Exocrine pancreas ; Male ; Medical sciences ; Methionine - pharmacology ; Other diseases. Semiology ; Oxidative Stress - drug effects ; Pharmacology. 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At present there is no effective and accepted therapy for NASH. The renin‐angiotensin system is involved in hepatic fibrosis through activation of hepatic stellate cells, major fibrogenic cells in the liver. Hepatic stellate cells are activated by liver injury to express excessive matrix proteins and profibrogenic cytokines such as transforming growth factor–beta 1. Medicines that inhibit this pathway may be of therapeutic potential in NASH. Using a methionine‐choline–deficient rat model of NASH, we studied the potential utility of an angiotensin II type 1 receptor blocker (ARB), olmesartan, on biochemical, histologic, and antioxidant measures of disease activity. ARB significantly attenuated increases in aspartate aminotransferase, activation of hepatic stellate cells, oxidative stress, expression of transforming growth factor–beta 1, expression of collagen genes, and liver fibrosis. Conclusion: Our observations strongly suggest a potential preventive role for ARB in the progression of nonalcoholic steatohepatitis. (HEPATOLOGY 2007.)</description><subject>Angiotensin II Type 1 Receptor Blockers - pharmacology</subject><subject>Animal Feed</subject><subject>Animals</subject><subject>Antibiotics. Antiinfectious agents. Antiparasitic agents</subject><subject>Antiseptics</subject><subject>Biological and medical sciences</subject><subject>Choline - pharmacology</subject><subject>Connective Tissue Growth Factor</subject><subject>Fatty Liver - drug therapy</subject><subject>Fatty Liver - pathology</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Imidazoles - pharmacology</subject><subject>Immediate-Early Proteins - metabolism</subject><subject>Intercellular Signaling Peptides and Proteins - metabolism</subject><subject>Liver Cirrhosis - drug therapy</subject><subject>Liver Cirrhosis - pathology</subject><subject>Liver Cirrhosis - prevention & control</subject><subject>Liver. Biliary tract. Portal circulation. Exocrine pancreas</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Methionine - pharmacology</subject><subject>Other diseases. Semiology</subject><subject>Oxidative Stress - drug effects</subject><subject>Pharmacology. Drug treatments</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Receptor, Angiotensin, Type 1 - metabolism</subject><subject>Tetrazoles - pharmacology</subject><subject>Transforming Growth Factor beta1 - metabolism</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><subject>Tumors</subject><issn>0270-9139</issn><issn>1527-3350</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kE1PwzAMhiMEgvFx4A-gXEDiUOYkTdsc0QRsEhIc4IZUpZnLAl1Tkkxo_57AJu3ExZbtR_brl5BzBjcMgI8XONxwVohqj4yY5GUmhIR9MgJeQqaYUEfkOIQPAFA5rw7JESslq0RRjcjbbf9uXcQ-2J7OZjSuB6SMejQ4ROdp0znziZ7afmEbGwNtbeNdsCF1qNeR9q7XnXEL11lDQ0QdXZKjo402nJKDVncBz7b5hLze371Mptnj08NscvuYGQGiynIJ87bMi6SqSCHnWqtcqRZKrtMERJFKQKmaVrBCIcuZLgRXoATKRrbihFxt9g7efa0wxHppg8Gu0z26VahLkAWXgifwegOa9EPw2NaDt0vt1zWD-tfKOmmv_6xM7MV26apZ4nxHbr1LwOUW0MHorvW6NzbsuKpiLJciceMN9207XP9_sZ7ePW9O_wBMLYme</recordid><startdate>200706</startdate><enddate>200706</enddate><creator>Hirose, Akira</creator><creator>Ono, Masafumi</creator><creator>Saibara, Toshiji</creator><creator>Nozaki, Yasuko</creator><creator>Masuda, Kosei</creator><creator>Yoshioka, Akemi</creator><creator>Takahashi, Masaya</creator><creator>Akisawa, Naoaki</creator><creator>Iwasaki, Shinji</creator><creator>Oben, Jude A.</creator><creator>Onishi, Saburo</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><general>Wiley</general><scope>IQODW</scope><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>7X8</scope></search><sort><creationdate>200706</creationdate><title>Angiotensin II type 1 receptor blocker inhibits fibrosis in rat nonalcoholic steatohepatitis</title><author>Hirose, Akira ; Ono, Masafumi ; Saibara, Toshiji ; Nozaki, Yasuko ; Masuda, Kosei ; Yoshioka, Akemi ; Takahashi, Masaya ; Akisawa, Naoaki ; Iwasaki, Shinji ; Oben, Jude A. ; Onishi, Saburo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3038-450df746175661742aa9499f072a0df0369490e59bf3169e141a6329093e5b5f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Angiotensin II Type 1 Receptor Blockers - pharmacology</topic><topic>Animal Feed</topic><topic>Animals</topic><topic>Antibiotics. Antiinfectious agents. Antiparasitic agents</topic><topic>Antiseptics</topic><topic>Biological and medical sciences</topic><topic>Choline - pharmacology</topic><topic>Connective Tissue Growth Factor</topic><topic>Fatty Liver - drug therapy</topic><topic>Fatty Liver - pathology</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Imidazoles - pharmacology</topic><topic>Immediate-Early Proteins - metabolism</topic><topic>Intercellular Signaling Peptides and Proteins - metabolism</topic><topic>Liver Cirrhosis - drug therapy</topic><topic>Liver Cirrhosis - pathology</topic><topic>Liver Cirrhosis - prevention & control</topic><topic>Liver. Biliary tract. Portal circulation. Exocrine pancreas</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Methionine - pharmacology</topic><topic>Other diseases. Semiology</topic><topic>Oxidative Stress - drug effects</topic><topic>Pharmacology. Drug treatments</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Receptor, Angiotensin, Type 1 - metabolism</topic><topic>Tetrazoles - pharmacology</topic><topic>Transforming Growth Factor beta1 - metabolism</topic><topic>Tumor Necrosis Factor-alpha - metabolism</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hirose, Akira</creatorcontrib><creatorcontrib>Ono, Masafumi</creatorcontrib><creatorcontrib>Saibara, Toshiji</creatorcontrib><creatorcontrib>Nozaki, Yasuko</creatorcontrib><creatorcontrib>Masuda, Kosei</creatorcontrib><creatorcontrib>Yoshioka, Akemi</creatorcontrib><creatorcontrib>Takahashi, Masaya</creatorcontrib><creatorcontrib>Akisawa, Naoaki</creatorcontrib><creatorcontrib>Iwasaki, Shinji</creatorcontrib><creatorcontrib>Oben, Jude A.</creatorcontrib><creatorcontrib>Onishi, Saburo</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Hepatology (Baltimore, Md.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hirose, Akira</au><au>Ono, Masafumi</au><au>Saibara, Toshiji</au><au>Nozaki, Yasuko</au><au>Masuda, Kosei</au><au>Yoshioka, Akemi</au><au>Takahashi, Masaya</au><au>Akisawa, Naoaki</au><au>Iwasaki, Shinji</au><au>Oben, Jude A.</au><au>Onishi, Saburo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Angiotensin II type 1 receptor blocker inhibits fibrosis in rat nonalcoholic steatohepatitis</atitle><jtitle>Hepatology (Baltimore, Md.)</jtitle><addtitle>Hepatology</addtitle><date>2007-06</date><risdate>2007</risdate><volume>45</volume><issue>6</issue><spage>1375</spage><epage>1381</epage><pages>1375-1381</pages><issn>0270-9139</issn><eissn>1527-3350</eissn><coden>HPTLD9</coden><abstract>Nonalcoholic steatohepatitis (NASH) is now the most frequent cause of chronic liver impairment in developed countries and is a suggested causative factor in the development of cryptogenic cirrhosis and hepatocellular carcinoma. At present there is no effective and accepted therapy for NASH. The renin‐angiotensin system is involved in hepatic fibrosis through activation of hepatic stellate cells, major fibrogenic cells in the liver. Hepatic stellate cells are activated by liver injury to express excessive matrix proteins and profibrogenic cytokines such as transforming growth factor–beta 1. Medicines that inhibit this pathway may be of therapeutic potential in NASH. Using a methionine‐choline–deficient rat model of NASH, we studied the potential utility of an angiotensin II type 1 receptor blocker (ARB), olmesartan, on biochemical, histologic, and antioxidant measures of disease activity. ARB significantly attenuated increases in aspartate aminotransferase, activation of hepatic stellate cells, oxidative stress, expression of transforming growth factor–beta 1, expression of collagen genes, and liver fibrosis. Conclusion: Our observations strongly suggest a potential preventive role for ARB in the progression of nonalcoholic steatohepatitis. (HEPATOLOGY 2007.)</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>17518368</pmid><doi>10.1002/hep.21638</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Angiotensin II Type 1 Receptor Blockers - pharmacology Animal Feed Animals Antibiotics. Antiinfectious agents. Antiparasitic agents Antiseptics Biological and medical sciences Choline - pharmacology Connective Tissue Growth Factor Fatty Liver - drug therapy Fatty Liver - pathology Gastroenterology. Liver. Pancreas. Abdomen Imidazoles - pharmacology Immediate-Early Proteins - metabolism Intercellular Signaling Peptides and Proteins - metabolism Liver Cirrhosis - drug therapy Liver Cirrhosis - pathology Liver Cirrhosis - prevention & control Liver. Biliary tract. Portal circulation. Exocrine pancreas Male Medical sciences Methionine - pharmacology Other diseases. Semiology Oxidative Stress - drug effects Pharmacology. Drug treatments Rats Rats, Wistar Receptor, Angiotensin, Type 1 - metabolism Tetrazoles - pharmacology Transforming Growth Factor beta1 - metabolism Tumor Necrosis Factor-alpha - metabolism Tumors |
| title | Angiotensin II type 1 receptor blocker inhibits fibrosis in rat nonalcoholic steatohepatitis |
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