Liver fibrosis in mice induced by carbon tetrachloride and its reversion by luteolin
Hepatic fibrosis is effusive wound healing process in which excessive connective tissue builds up in the liver. Because specific treatments to stop progressive fibrosis of the liver are not available, we have investigated the effects of luteolin on carbon tetrachloride (CCl 4)-induced hepatic fibros...
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| Veröffentlicht in: | Toxicology and applied pharmacology 2009-12, Vol.241 (3), p.311-321 |
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| description | Hepatic fibrosis is effusive wound healing process in which excessive connective tissue builds up in the liver. Because specific treatments to stop progressive fibrosis of the liver are not available, we have investigated the effects of luteolin on carbon tetrachloride (CCl
4)-induced hepatic fibrosis. Male Balb/C mice were treated with CCl
4 (0.4 ml/kg) intraperitoneally (i.p.), twice a week for 6 weeks. Luteolin was administered i.p. once daily for next 2 weeks, in doses of 10, 25, and 50 mg/kg of body weight. The CCl
4 control group has been observed for spontaneous reversion of fibrosis. CCl
4-intoxication increased serum aminotransferase and alkaline phosphatase levels and disturbed hepatic antioxidative status. Most of these parameters were spontaneously normalized in the CCl
4 control group, although the progression of liver fibrosis was observed histologically. Luteolin treatment has increased hepatic matrix metalloproteinase-9 levels and metallothionein (MT) I/II expression, eliminated fibrinous deposits and restored architecture of the liver in a dose-dependent manner. Concomitantly, the expression of glial fibrillary acidic protein and α-smooth muscle actin indicated deactivation of hepatic stellate cells. Our results suggest the therapeutic effects of luteolin on CCl
4-induced liver fibrosis by promoting extracellular matrix degradation in the fibrotic liver tissue and the strong enhancement of hepatic regenerative capability, with MTs as a critical mediator of liver regeneration. |
| doi_str_mv | 10.1016/j.taap.2009.09.001 |
| format | Article |
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4)-induced hepatic fibrosis. Male Balb/C mice were treated with CCl
4 (0.4 ml/kg) intraperitoneally (i.p.), twice a week for 6 weeks. Luteolin was administered i.p. once daily for next 2 weeks, in doses of 10, 25, and 50 mg/kg of body weight. The CCl
4 control group has been observed for spontaneous reversion of fibrosis. CCl
4-intoxication increased serum aminotransferase and alkaline phosphatase levels and disturbed hepatic antioxidative status. Most of these parameters were spontaneously normalized in the CCl
4 control group, although the progression of liver fibrosis was observed histologically. Luteolin treatment has increased hepatic matrix metalloproteinase-9 levels and metallothionein (MT) I/II expression, eliminated fibrinous deposits and restored architecture of the liver in a dose-dependent manner. Concomitantly, the expression of glial fibrillary acidic protein and α-smooth muscle actin indicated deactivation of hepatic stellate cells. Our results suggest the therapeutic effects of luteolin on CCl
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4)-induced hepatic fibrosis. Male Balb/C mice were treated with CCl
4 (0.4 ml/kg) intraperitoneally (i.p.), twice a week for 6 weeks. Luteolin was administered i.p. once daily for next 2 weeks, in doses of 10, 25, and 50 mg/kg of body weight. The CCl
4 control group has been observed for spontaneous reversion of fibrosis. CCl
4-intoxication increased serum aminotransferase and alkaline phosphatase levels and disturbed hepatic antioxidative status. Most of these parameters were spontaneously normalized in the CCl
4 control group, although the progression of liver fibrosis was observed histologically. Luteolin treatment has increased hepatic matrix metalloproteinase-9 levels and metallothionein (MT) I/II expression, eliminated fibrinous deposits and restored architecture of the liver in a dose-dependent manner. Concomitantly, the expression of glial fibrillary acidic protein and α-smooth muscle actin indicated deactivation of hepatic stellate cells. Our results suggest the therapeutic effects of luteolin on CCl
4-induced liver fibrosis by promoting extracellular matrix degradation in the fibrotic liver tissue and the strong enhancement of hepatic regenerative capability, with MTs as a critical mediator of liver regeneration.</description><subject>60 APPLIED LIFE SCIENCES</subject><subject>ACTIN</subject><subject>Actins - metabolism</subject><subject>ALKALINE PHOSPHATASE</subject><subject>ANIMAL TISSUES</subject><subject>ANIMALS</subject><subject>Biological and medical sciences</subject><subject>BIOLOGICAL RECOVERY</subject><subject>BODY</subject><subject>CARBON TETRACHLORIDE</subject><subject>Carbon Tetrachloride Poisoning - drug therapy</subject><subject>Carbon Tetrachloride Poisoning - pathology</subject><subject>Chemical and Drug Induced Liver Injury - pathology</subject><subject>CHLORINATED ALIPHATIC HYDROCARBONS</subject><subject>CONNECTIVE TISSUE</subject><subject>Copper - metabolism</subject><subject>DIGESTIVE SYSTEM</subject><subject>DOSES</subject><subject>ENZYMES</subject><subject>ESTERASES</subject><subject>Expectorants - therapeutic use</subject><subject>FIBROSIS</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>GLANDS</subject><subject>Glial fibrillary acidic protein</subject><subject>Glial Fibrillary Acidic Protein - metabolism</subject><subject>Glutathione - metabolism</subject><subject>HALOGENATED ALIPHATIC HYDROCARBONS</subject><subject>HEALING</subject><subject>HYDROLASES</subject><subject>Hydroxyproline - metabolism</subject><subject>Immunohistochemistry</subject><subject>LIVER</subject><subject>Liver - metabolism</subject><subject>Liver - pathology</subject><subject>Liver Cirrhosis - chemically induced</subject><subject>Liver Cirrhosis - drug therapy</subject><subject>Liver Cirrhosis - pathology</subject><subject>Liver fibrosis</subject><subject>Liver. Biliary tract. Portal circulation. Exocrine pancreas</subject><subject>Luteolin</subject><subject>Luteolin - therapeutic use</subject><subject>Male</subject><subject>MAMMALS</subject><subject>Matrix metalloproteinase</subject><subject>Matrix Metalloproteinases - metabolism</subject><subject>Medical sciences</subject><subject>METALLOPROTEINS</subject><subject>METALLOTHIONEIN</subject><subject>Metallothionein - metabolism</subject><subject>MICE</subject><subject>Mice, Inbred BALB C</subject><subject>MUSCLES</subject><subject>ORGANIC CHLORINE COMPOUNDS</subject><subject>ORGANIC COMPOUNDS</subject><subject>ORGANIC HALOGEN COMPOUNDS</subject><subject>ORGANS</subject><subject>Other diseases. Semiology</subject><subject>PATHOLOGICAL CHANGES</subject><subject>PHOSPHATASES</subject><subject>PROTEINS</subject><subject>RODENTS</subject><subject>Superoxide Dismutase - metabolism</subject><subject>TOXICITY</subject><subject>Toxicology</subject><subject>VERTEBRATES</subject><subject>Vitamin A - metabolism</subject><subject>Zinc - metabolism</subject><subject>α-Smooth muscle actin</subject><issn>0041-008X</issn><issn>1096-0333</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kU9r3DAQxUVpaTbbfIEeiqE0N29mJHttQS8h9B8s9JJAb0KWRkSLV95KciDfvnJ2aW9FA3OY3zzmPTH2HmGDgNub_SZrfdxwALlZCvAVWyHIbQ1CiNdsBdBgDdD_umCXKe2hgE2Db9kFyq7pWsAVu9_5J4qV80Ockk-VD9XBGyrdzoZsNTxXRsdhClWmHLV5HKfoLVU62MrnVEUq68mXeSHHOdM0-vCOvXF6THR17mv28PXL_d33evfz24-7211tWoRcWwktDoNuTculddveOjCakCSg6FouhOm0kdLhUEyBc22_JeTdIIiDRC7W7ONJd0rZq2R8JvNophDIZMVRNE2PTaGuT9QxTr9nSlkdfDI0jjrQNKcClide5PgJNCWLFMmpY_QHHZ8VgloSV3u1JK6WxNVS5c41-3BWn4cD2X8r54gL8OkM6GT06KIOxqe_HOfYdn0Dhft84qgk9uQpLoYolE_wcfFjJ_-_O_4AY6ueKg</recordid><startdate>20091215</startdate><enddate>20091215</enddate><creator>Domitrović, Robert</creator><creator>Jakovac, Hrvoje</creator><creator>Tomac, Jelena</creator><creator>Šain, Ivana</creator><general>Elsevier Inc</general><general>Elsevier</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>7U7</scope><scope>C1K</scope><scope>OTOTI</scope></search><sort><creationdate>20091215</creationdate><title>Liver fibrosis in mice induced by carbon tetrachloride and its reversion by luteolin</title><author>Domitrović, Robert ; Jakovac, Hrvoje ; Tomac, Jelena ; Šain, Ivana</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c510t-d9051bba5c529df68df0cae1e901375233c7ac99f1b0960ff586e127b3e209123</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>60 APPLIED LIFE SCIENCES</topic><topic>ACTIN</topic><topic>Actins - metabolism</topic><topic>ALKALINE PHOSPHATASE</topic><topic>ANIMAL TISSUES</topic><topic>ANIMALS</topic><topic>Biological and medical sciences</topic><topic>BIOLOGICAL RECOVERY</topic><topic>BODY</topic><topic>CARBON TETRACHLORIDE</topic><topic>Carbon Tetrachloride Poisoning - drug therapy</topic><topic>Carbon Tetrachloride Poisoning - pathology</topic><topic>Chemical and Drug Induced Liver Injury - pathology</topic><topic>CHLORINATED ALIPHATIC HYDROCARBONS</topic><topic>CONNECTIVE TISSUE</topic><topic>Copper - metabolism</topic><topic>DIGESTIVE SYSTEM</topic><topic>DOSES</topic><topic>ENZYMES</topic><topic>ESTERASES</topic><topic>Expectorants - therapeutic use</topic><topic>FIBROSIS</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>GLANDS</topic><topic>Glial fibrillary acidic protein</topic><topic>Glial Fibrillary Acidic Protein - metabolism</topic><topic>Glutathione - metabolism</topic><topic>HALOGENATED ALIPHATIC HYDROCARBONS</topic><topic>HEALING</topic><topic>HYDROLASES</topic><topic>Hydroxyproline - metabolism</topic><topic>Immunohistochemistry</topic><topic>LIVER</topic><topic>Liver - metabolism</topic><topic>Liver - pathology</topic><topic>Liver Cirrhosis - chemically induced</topic><topic>Liver Cirrhosis - drug therapy</topic><topic>Liver Cirrhosis - pathology</topic><topic>Liver fibrosis</topic><topic>Liver. Biliary tract. Portal circulation. Exocrine pancreas</topic><topic>Luteolin</topic><topic>Luteolin - therapeutic use</topic><topic>Male</topic><topic>MAMMALS</topic><topic>Matrix metalloproteinase</topic><topic>Matrix Metalloproteinases - metabolism</topic><topic>Medical sciences</topic><topic>METALLOPROTEINS</topic><topic>METALLOTHIONEIN</topic><topic>Metallothionein - metabolism</topic><topic>MICE</topic><topic>Mice, Inbred BALB C</topic><topic>MUSCLES</topic><topic>ORGANIC CHLORINE COMPOUNDS</topic><topic>ORGANIC COMPOUNDS</topic><topic>ORGANIC HALOGEN COMPOUNDS</topic><topic>ORGANS</topic><topic>Other diseases. Semiology</topic><topic>PATHOLOGICAL CHANGES</topic><topic>PHOSPHATASES</topic><topic>PROTEINS</topic><topic>RODENTS</topic><topic>Superoxide Dismutase - metabolism</topic><topic>TOXICITY</topic><topic>Toxicology</topic><topic>VERTEBRATES</topic><topic>Vitamin A - metabolism</topic><topic>Zinc - metabolism</topic><topic>α-Smooth muscle actin</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Domitrović, Robert</creatorcontrib><creatorcontrib>Jakovac, Hrvoje</creatorcontrib><creatorcontrib>Tomac, Jelena</creatorcontrib><creatorcontrib>Šain, Ivana</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>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>OSTI.GOV</collection><jtitle>Toxicology and applied pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Domitrović, Robert</au><au>Jakovac, Hrvoje</au><au>Tomac, Jelena</au><au>Šain, Ivana</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Liver fibrosis in mice induced by carbon tetrachloride and its reversion by luteolin</atitle><jtitle>Toxicology and applied pharmacology</jtitle><addtitle>Toxicol Appl Pharmacol</addtitle><date>2009-12-15</date><risdate>2009</risdate><volume>241</volume><issue>3</issue><spage>311</spage><epage>321</epage><pages>311-321</pages><issn>0041-008X</issn><eissn>1096-0333</eissn><coden>TXAPA9</coden><abstract>Hepatic fibrosis is effusive wound healing process in which excessive connective tissue builds up in the liver. Because specific treatments to stop progressive fibrosis of the liver are not available, we have investigated the effects of luteolin on carbon tetrachloride (CCl
4)-induced hepatic fibrosis. Male Balb/C mice were treated with CCl
4 (0.4 ml/kg) intraperitoneally (i.p.), twice a week for 6 weeks. Luteolin was administered i.p. once daily for next 2 weeks, in doses of 10, 25, and 50 mg/kg of body weight. The CCl
4 control group has been observed for spontaneous reversion of fibrosis. CCl
4-intoxication increased serum aminotransferase and alkaline phosphatase levels and disturbed hepatic antioxidative status. Most of these parameters were spontaneously normalized in the CCl
4 control group, although the progression of liver fibrosis was observed histologically. Luteolin treatment has increased hepatic matrix metalloproteinase-9 levels and metallothionein (MT) I/II expression, eliminated fibrinous deposits and restored architecture of the liver in a dose-dependent manner. Concomitantly, the expression of glial fibrillary acidic protein and α-smooth muscle actin indicated deactivation of hepatic stellate cells. Our results suggest the therapeutic effects of luteolin on CCl
4-induced liver fibrosis by promoting extracellular matrix degradation in the fibrotic liver tissue and the strong enhancement of hepatic regenerative capability, with MTs as a critical mediator of liver regeneration.</abstract><cop>Amsterdam</cop><pub>Elsevier Inc</pub><pmid>19747501</pmid><doi>10.1016/j.taap.2009.09.001</doi><tpages>11</tpages></addata></record> |
| fulltext | fulltext |
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| ispartof | Toxicology and applied pharmacology, 2009-12, Vol.241 (3), p.311-321 |
| issn | 0041-008X 1096-0333 |
| language | eng |
| recordid | cdi_osti_scitechconnect_21344814 |
| source | MEDLINE; Elsevier ScienceDirect Journals |
| subjects | 60 APPLIED LIFE SCIENCES ACTIN Actins - metabolism ALKALINE PHOSPHATASE ANIMAL TISSUES ANIMALS Biological and medical sciences BIOLOGICAL RECOVERY BODY CARBON TETRACHLORIDE Carbon Tetrachloride Poisoning - drug therapy Carbon Tetrachloride Poisoning - pathology Chemical and Drug Induced Liver Injury - pathology CHLORINATED ALIPHATIC HYDROCARBONS CONNECTIVE TISSUE Copper - metabolism DIGESTIVE SYSTEM DOSES ENZYMES ESTERASES Expectorants - therapeutic use FIBROSIS Gastroenterology. Liver. Pancreas. Abdomen GLANDS Glial fibrillary acidic protein Glial Fibrillary Acidic Protein - metabolism Glutathione - metabolism HALOGENATED ALIPHATIC HYDROCARBONS HEALING HYDROLASES Hydroxyproline - metabolism Immunohistochemistry LIVER Liver - metabolism Liver - pathology Liver Cirrhosis - chemically induced Liver Cirrhosis - drug therapy Liver Cirrhosis - pathology Liver fibrosis Liver. Biliary tract. Portal circulation. Exocrine pancreas Luteolin Luteolin - therapeutic use Male MAMMALS Matrix metalloproteinase Matrix Metalloproteinases - metabolism Medical sciences METALLOPROTEINS METALLOTHIONEIN Metallothionein - metabolism MICE Mice, Inbred BALB C MUSCLES ORGANIC CHLORINE COMPOUNDS ORGANIC COMPOUNDS ORGANIC HALOGEN COMPOUNDS ORGANS Other diseases. Semiology PATHOLOGICAL CHANGES PHOSPHATASES PROTEINS RODENTS Superoxide Dismutase - metabolism TOXICITY Toxicology VERTEBRATES Vitamin A - metabolism Zinc - metabolism α-Smooth muscle actin |
| title | Liver fibrosis in mice induced by carbon tetrachloride and its reversion by luteolin |
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