Hepatoprotective effects of geniposide in a rat model of nonalcoholic steatohepatitis
Objectives Nonalcoholic steatohepatitis (NASH), a metabolic disorder of the liver, may gradually evolve into fibrosis or cirrhosis. Recent studies have suggested that geniposide can effectively inhibit experimental liver fibrosis. Therefore, the aim of this study was to determine whether geniposide...
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description | Objectives Nonalcoholic steatohepatitis (NASH), a metabolic disorder of the liver, may gradually evolve into fibrosis or cirrhosis. Recent studies have suggested that geniposide can effectively inhibit experimental liver fibrosis. Therefore, the aim of this study was to determine whether geniposide can influence the early phase of fibrogenesis in an animal model of NASH.
Methods Male Sprague–Dawley rats were given a high fat diet alone or the same diet combined with geniposide at doses of 25, 50 or 100 mg/kg for six weeks. Ten rats received corresponding solvent as a normal control.
Key findings Treatment with geniposide could improve liver histology through reducing the elevated liver index (liver weight/body weight), serum alanine aminotransferase and aspartate aminotransferase. Total cholesterol, triglycerides and free fatty acids in serum and liver decreased in geniposide‐treated rats. Furthermore, geniposide increased serum insulin levels but reduced serum tumour necrosis factor‐α level in high‐fat diet rats. In addition, geniposide suppressed expression of CYP2E1 and increased peroxisome proliferator‐activated receptor‐α (PPARα) expression. These benefits may be associated with increased superoxide dismutase and decreased malondialdehyde in liver.
Conclusions Geniposide exerts protective effects against hepatic steatosis in rats fed with a high fat diet; the underlying mechanism may be associated with its antioxidant actions or regulation of adipocytokine release and expression of PPARα. |
doi_str_mv | 10.1111/j.2042-7158.2011.01256.x |
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Methods Male Sprague–Dawley rats were given a high fat diet alone or the same diet combined with geniposide at doses of 25, 50 or 100 mg/kg for six weeks. Ten rats received corresponding solvent as a normal control.
Key findings Treatment with geniposide could improve liver histology through reducing the elevated liver index (liver weight/body weight), serum alanine aminotransferase and aspartate aminotransferase. Total cholesterol, triglycerides and free fatty acids in serum and liver decreased in geniposide‐treated rats. Furthermore, geniposide increased serum insulin levels but reduced serum tumour necrosis factor‐α level in high‐fat diet rats. In addition, geniposide suppressed expression of CYP2E1 and increased peroxisome proliferator‐activated receptor‐α (PPARα) expression. These benefits may be associated with increased superoxide dismutase and decreased malondialdehyde in liver.
Conclusions Geniposide exerts protective effects against hepatic steatosis in rats fed with a high fat diet; the underlying mechanism may be associated with its antioxidant actions or regulation of adipocytokine release and expression of PPARα.</description><identifier>ISSN: 0022-3573</identifier><identifier>EISSN: 2042-7158</identifier><identifier>DOI: 10.1111/j.2042-7158.2011.01256.x</identifier><identifier>PMID: 21401612</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Alanine Transaminase - blood ; Animals ; Anti-Inflammatory Agents - pharmacology ; Anti-Inflammatory Agents - therapeutic use ; Aspartate Aminotransferases - blood ; Cytochrome P-450 CYP2E1 - biosynthesis ; Dietary Fats - adverse effects ; Disease Models, Animal ; Dose-Response Relationship, Drug ; Drug Evaluation, Preclinical ; Fatty Liver - etiology ; Fatty Liver - metabolism ; Fatty Liver - prevention & control ; geniposide ; Insulin - blood ; Iridoids - pharmacology ; Iridoids - therapeutic use ; Lipid Metabolism - drug effects ; lipid peroxidation ; Male ; Malondialdehyde - metabolism ; Non-alcoholic Fatty Liver Disease ; non-alcoholic steatohepatitis (NASH) ; PPAR alpha - biosynthesis ; Rats ; Rats, Sprague-Dawley ; Superoxide Dismutase - metabolism ; Tumor Necrosis Factor-alpha - blood</subject><ispartof>Journal of pharmacy and pharmacology, 2011-04, Vol.63 (4), p.587-593</ispartof><rights>2011 The Authors. JPP © 2011 Royal Pharmaceutical Society</rights><rights>2011 The Authors. JPP © 2011 Royal Pharmaceutical Society.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5236-f195030cc184289034c4e6dd5e03338fbe84b05ab217838cd96cb88ccf3088f13</citedby><cites>FETCH-LOGICAL-c5236-f195030cc184289034c4e6dd5e03338fbe84b05ab217838cd96cb88ccf3088f13</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fj.2042-7158.2011.01256.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.2042-7158.2011.01256.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1416,27923,27924,45573,45574</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21401612$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ma, Taotao</creatorcontrib><creatorcontrib>Huang, Cheng</creatorcontrib><creatorcontrib>Zong, Guojun</creatorcontrib><creatorcontrib>Zha, Dajun</creatorcontrib><creatorcontrib>Meng, Xiaoming</creatorcontrib><creatorcontrib>Li, Jun</creatorcontrib><creatorcontrib>Tang, Wenjian</creatorcontrib><title>Hepatoprotective effects of geniposide in a rat model of nonalcoholic steatohepatitis</title><title>Journal of pharmacy and pharmacology</title><addtitle>J Pharm Pharmacol</addtitle><description>Objectives Nonalcoholic steatohepatitis (NASH), a metabolic disorder of the liver, may gradually evolve into fibrosis or cirrhosis. Recent studies have suggested that geniposide can effectively inhibit experimental liver fibrosis. Therefore, the aim of this study was to determine whether geniposide can influence the early phase of fibrogenesis in an animal model of NASH.
Methods Male Sprague–Dawley rats were given a high fat diet alone or the same diet combined with geniposide at doses of 25, 50 or 100 mg/kg for six weeks. Ten rats received corresponding solvent as a normal control.
Key findings Treatment with geniposide could improve liver histology through reducing the elevated liver index (liver weight/body weight), serum alanine aminotransferase and aspartate aminotransferase. Total cholesterol, triglycerides and free fatty acids in serum and liver decreased in geniposide‐treated rats. Furthermore, geniposide increased serum insulin levels but reduced serum tumour necrosis factor‐α level in high‐fat diet rats. In addition, geniposide suppressed expression of CYP2E1 and increased peroxisome proliferator‐activated receptor‐α (PPARα) expression. These benefits may be associated with increased superoxide dismutase and decreased malondialdehyde in liver.
Conclusions Geniposide exerts protective effects against hepatic steatosis in rats fed with a high fat diet; the underlying mechanism may be associated with its antioxidant actions or regulation of adipocytokine release and expression of PPARα.</description><subject>Alanine Transaminase - blood</subject><subject>Animals</subject><subject>Anti-Inflammatory Agents - pharmacology</subject><subject>Anti-Inflammatory Agents - therapeutic use</subject><subject>Aspartate Aminotransferases - blood</subject><subject>Cytochrome P-450 CYP2E1 - biosynthesis</subject><subject>Dietary Fats - adverse effects</subject><subject>Disease Models, Animal</subject><subject>Dose-Response Relationship, Drug</subject><subject>Drug Evaluation, Preclinical</subject><subject>Fatty Liver - etiology</subject><subject>Fatty Liver - metabolism</subject><subject>Fatty Liver - prevention & control</subject><subject>geniposide</subject><subject>Insulin - blood</subject><subject>Iridoids - pharmacology</subject><subject>Iridoids - therapeutic use</subject><subject>Lipid Metabolism - drug effects</subject><subject>lipid peroxidation</subject><subject>Male</subject><subject>Malondialdehyde - metabolism</subject><subject>Non-alcoholic Fatty Liver Disease</subject><subject>non-alcoholic steatohepatitis (NASH)</subject><subject>PPAR alpha - biosynthesis</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Superoxide Dismutase - metabolism</subject><subject>Tumor Necrosis Factor-alpha - blood</subject><issn>0022-3573</issn><issn>2042-7158</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkMFuEzEURa0K1IbSX6i8YzXh2R57nE2lKtAGFIUsWrG0PJ5n6jAZh_GEpn-Ph5Ss8cZXevcdW4cQymDK8vm4mXIoeVExqXNibAqMSzU9nJHJafCGTAA4L4SsxAV5l9IGACql1Dm54KwEphifkMcF7uwQd30c0A3hN1L0PqdEo6c_sAu7mEKDNHTU0t4OdBsbbMdhFzvbuvgU2-BoGjBTnkZWGEJ6T9562ya8er0vyePd54f5olh-u_8yv10WTnKhCs9mEgQ4x3TJ9QxE6UpUTSMRhBDa16jLGqStOau00K6ZKVdr7ZwXoLVn4pJ8OHLz_3_tMQ1mG5LDtrUdxn0yWlaZy0Dnpj42XR9T6tGbXR-2tn8xDMzo1GzMqM6M6szo1Px1ag559fr1kX29xea0-E9iLtwcC8-hxZf_Bpuv68V6jBlQHAEhezycALb_aVQlKmm-r-7NSj-slp_Wc1OKP0galNA</recordid><startdate>201104</startdate><enddate>201104</enddate><creator>Ma, Taotao</creator><creator>Huang, Cheng</creator><creator>Zong, Guojun</creator><creator>Zha, Dajun</creator><creator>Meng, Xiaoming</creator><creator>Li, Jun</creator><creator>Tang, Wenjian</creator><general>Blackwell Publishing Ltd</general><scope>BSCLL</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>201104</creationdate><title>Hepatoprotective effects of geniposide in a rat model of nonalcoholic steatohepatitis</title><author>Ma, Taotao ; Huang, Cheng ; Zong, Guojun ; Zha, Dajun ; Meng, Xiaoming ; Li, Jun ; Tang, Wenjian</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5236-f195030cc184289034c4e6dd5e03338fbe84b05ab217838cd96cb88ccf3088f13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Alanine Transaminase - blood</topic><topic>Animals</topic><topic>Anti-Inflammatory Agents - pharmacology</topic><topic>Anti-Inflammatory Agents - therapeutic use</topic><topic>Aspartate Aminotransferases - blood</topic><topic>Cytochrome P-450 CYP2E1 - biosynthesis</topic><topic>Dietary Fats - adverse effects</topic><topic>Disease Models, Animal</topic><topic>Dose-Response Relationship, Drug</topic><topic>Drug Evaluation, Preclinical</topic><topic>Fatty Liver - etiology</topic><topic>Fatty Liver - metabolism</topic><topic>Fatty Liver - prevention & control</topic><topic>geniposide</topic><topic>Insulin - blood</topic><topic>Iridoids - pharmacology</topic><topic>Iridoids - therapeutic use</topic><topic>Lipid Metabolism - drug effects</topic><topic>lipid peroxidation</topic><topic>Male</topic><topic>Malondialdehyde - metabolism</topic><topic>Non-alcoholic Fatty Liver Disease</topic><topic>non-alcoholic steatohepatitis (NASH)</topic><topic>PPAR alpha - biosynthesis</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Superoxide Dismutase - metabolism</topic><topic>Tumor Necrosis Factor-alpha - blood</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ma, Taotao</creatorcontrib><creatorcontrib>Huang, Cheng</creatorcontrib><creatorcontrib>Zong, Guojun</creatorcontrib><creatorcontrib>Zha, Dajun</creatorcontrib><creatorcontrib>Meng, Xiaoming</creatorcontrib><creatorcontrib>Li, Jun</creatorcontrib><creatorcontrib>Tang, Wenjian</creatorcontrib><collection>Istex</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>Journal of pharmacy and pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ma, Taotao</au><au>Huang, Cheng</au><au>Zong, Guojun</au><au>Zha, Dajun</au><au>Meng, Xiaoming</au><au>Li, Jun</au><au>Tang, Wenjian</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Hepatoprotective effects of geniposide in a rat model of nonalcoholic steatohepatitis</atitle><jtitle>Journal of pharmacy and pharmacology</jtitle><addtitle>J Pharm Pharmacol</addtitle><date>2011-04</date><risdate>2011</risdate><volume>63</volume><issue>4</issue><spage>587</spage><epage>593</epage><pages>587-593</pages><issn>0022-3573</issn><eissn>2042-7158</eissn><abstract>Objectives Nonalcoholic steatohepatitis (NASH), a metabolic disorder of the liver, may gradually evolve into fibrosis or cirrhosis. Recent studies have suggested that geniposide can effectively inhibit experimental liver fibrosis. Therefore, the aim of this study was to determine whether geniposide can influence the early phase of fibrogenesis in an animal model of NASH.
Methods Male Sprague–Dawley rats were given a high fat diet alone or the same diet combined with geniposide at doses of 25, 50 or 100 mg/kg for six weeks. Ten rats received corresponding solvent as a normal control.
Key findings Treatment with geniposide could improve liver histology through reducing the elevated liver index (liver weight/body weight), serum alanine aminotransferase and aspartate aminotransferase. Total cholesterol, triglycerides and free fatty acids in serum and liver decreased in geniposide‐treated rats. Furthermore, geniposide increased serum insulin levels but reduced serum tumour necrosis factor‐α level in high‐fat diet rats. In addition, geniposide suppressed expression of CYP2E1 and increased peroxisome proliferator‐activated receptor‐α (PPARα) expression. These benefits may be associated with increased superoxide dismutase and decreased malondialdehyde in liver.
Conclusions Geniposide exerts protective effects against hepatic steatosis in rats fed with a high fat diet; the underlying mechanism may be associated with its antioxidant actions or regulation of adipocytokine release and expression of PPARα.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>21401612</pmid><doi>10.1111/j.2042-7158.2011.01256.x</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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source | MEDLINE; Oxford University Press Journals All Titles (1996-Current); Wiley Online Library All Journals |
subjects | Alanine Transaminase - blood Animals Anti-Inflammatory Agents - pharmacology Anti-Inflammatory Agents - therapeutic use Aspartate Aminotransferases - blood Cytochrome P-450 CYP2E1 - biosynthesis Dietary Fats - adverse effects Disease Models, Animal Dose-Response Relationship, Drug Drug Evaluation, Preclinical Fatty Liver - etiology Fatty Liver - metabolism Fatty Liver - prevention & control geniposide Insulin - blood Iridoids - pharmacology Iridoids - therapeutic use Lipid Metabolism - drug effects lipid peroxidation Male Malondialdehyde - metabolism Non-alcoholic Fatty Liver Disease non-alcoholic steatohepatitis (NASH) PPAR alpha - biosynthesis Rats Rats, Sprague-Dawley Superoxide Dismutase - metabolism Tumor Necrosis Factor-alpha - blood |
title | Hepatoprotective effects of geniposide in a rat model of nonalcoholic steatohepatitis |
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