Platelets prevent acute hepatitis induced by anti-fas antibody
Background and Aim: Platelets provide many functions in the body, especially to the liver. The purpose of this study is to investigate the effect of thrombocytosis with acute hepatitis induced by anti‐Fas antibody and its mechanism. Methods: Acute hepatitis was induced by administration of anti‐Fa...
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| Veröffentlicht in: | Journal of gastroenterology and hepatology 2011-02, Vol.26 (2), p.348-355 |
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| creator | Hisakura, Katsuji Murata, Soichiro Takahashi, Kazuhiro Matsuo, Ryota Pak, Sugiru Ikeda, Naoya Kawasaki, Takuya Kohno, Keisuke Myronovych, Andriy Nakano, Yoritaka Ikeda, Osamu Watanabe, Motonobu Ohkohchi, Nobuhiro |
| description | Background and Aim: Platelets provide many functions in the body, especially to the liver. The purpose of this study is to investigate the effect of thrombocytosis with acute hepatitis induced by anti‐Fas antibody and its mechanism.
Methods: Acute hepatitis was induced by administration of anti‐Fas antibody in normal and thrombocytotic C57BL6J mice. For thrombocytosis, thrombopoietin; PEG‐rHuMGDF was injected 5 days before and just prior to administration of anti‐Fas antibody. To investigate the mechanisms, hepatocyte cell line (AML12) and sinusoidal endothelial cell line (M1) were induced apoptosis by staurosporine. They were cultured with platelets or thrombopoietin. Examination items were as follows: platelet number, alanine aminotransferase (ALT), histological findings, TUNEL (TdT‐mediated dUTP‐biotin Nick End Labeling) staining, and the expression of proteins associated with apoptosis in vivo and in vitro.
Results: Platelets were significantly increased in the thrombocytotic group (P |
| doi_str_mv | 10.1111/j.1440-1746.2010.06334.x |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_847435787</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>847435787</sourcerecordid><originalsourceid>FETCH-LOGICAL-c5854-9335ee104f01c48faea2532c8585474f13d4c5030ce3148751e0dc767cc1218b3</originalsourceid><addsrcrecordid>eNqNkE1vEzEQhi1ERUPhL6C9IHrZdMYfa-cAEqpKSqmAQwGJi-V4Z4XDZhPWXkj-Pd4mhBvCF488zzsePYwVCFPM52I5RSmhRC2rKYf8CpUQcrp9wCbHxkM2AYOqnAmcnbLHMS4BQIJWj9gpR16h5tWEvfrYukQtpVhsevpJXSqcHxIV32jjUkghFqGrB091sdgVrkuhbFy8LxbreveEnTSujfT0cJ-xT2-u7i6vy9sP87eXr29Lr4ySeQehiBBkA-ilaRw5rgT3Zuxq2aCopVcgwJNAabRCgtrrSnuPHM1CnLEX-7mbfv1joJjsKkRPbes6Wg_RmjxFKG10Js__SSJwMEpxgxk1e9T36xh7auymDyvX7zJkR892aUeddtRpR8_23rPd5uizwy_DYkX1MfhHbAaeHwAXvWub3nU-xL-cMIh5VuZe7rlfoaXdfy9gb-bXY5Xz5T4fYqLtMe_677bSQiv75f3cwuzu3Q1-_WyN-A3QVqVw</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1020855281</pqid></control><display><type>article</type><title>Platelets prevent acute hepatitis induced by anti-fas antibody</title><source>MEDLINE</source><source>Wiley Online Library Journals Frontfile Complete</source><creator>Hisakura, Katsuji ; Murata, Soichiro ; Takahashi, Kazuhiro ; Matsuo, Ryota ; Pak, Sugiru ; Ikeda, Naoya ; Kawasaki, Takuya ; Kohno, Keisuke ; Myronovych, Andriy ; Nakano, Yoritaka ; Ikeda, Osamu ; Watanabe, Motonobu ; Ohkohchi, Nobuhiro</creator><creatorcontrib>Hisakura, Katsuji ; Murata, Soichiro ; Takahashi, Kazuhiro ; Matsuo, Ryota ; Pak, Sugiru ; Ikeda, Naoya ; Kawasaki, Takuya ; Kohno, Keisuke ; Myronovych, Andriy ; Nakano, Yoritaka ; Ikeda, Osamu ; Watanabe, Motonobu ; Ohkohchi, Nobuhiro</creatorcontrib><description>Background and Aim: Platelets provide many functions in the body, especially to the liver. The purpose of this study is to investigate the effect of thrombocytosis with acute hepatitis induced by anti‐Fas antibody and its mechanism.
Methods: Acute hepatitis was induced by administration of anti‐Fas antibody in normal and thrombocytotic C57BL6J mice. For thrombocytosis, thrombopoietin; PEG‐rHuMGDF was injected 5 days before and just prior to administration of anti‐Fas antibody. To investigate the mechanisms, hepatocyte cell line (AML12) and sinusoidal endothelial cell line (M1) were induced apoptosis by staurosporine. They were cultured with platelets or thrombopoietin. Examination items were as follows: platelet number, alanine aminotransferase (ALT), histological findings, TUNEL (TdT‐mediated dUTP‐biotin Nick End Labeling) staining, and the expression of proteins associated with apoptosis in vivo and in vitro.
Results: Platelets were significantly increased in the thrombocytotic group (P < 0.01). Serum ALT levels were significantly reduced by thrombocytosis at 6, 24 and 72 h after the administration (P < 0.05). In histological findings, hemorrhagic necrosis was observed in the normal group, but not observed in the thrombocytotic group. TUNEL‐positive hepatocytes were reduced and the expression of cleaved caspase‐3 was significantly decreased in the thrombocytotic group. The phosphorylation of Akt, the increment of Bcl‐xL and the decrease of cleaved caspase‐3 were observed in AML12 cells cultured with platelets, but were not observed cultured with thrombopoietin. Platelets and thrombopoietin had no anti‐apoptotic effect on M1 cells.
Conclusion: Increase of platelets has a preventative effect against acute hepatitis induced by the anti‐Fas antibody. It is suggested that platelets have a direct protective effect against apoptosis of hepatocytes.</description><identifier>ISSN: 0815-9319</identifier><identifier>EISSN: 1440-1746</identifier><identifier>DOI: 10.1111/j.1440-1746.2010.06334.x</identifier><identifier>PMID: 21261726</identifier><language>eng</language><publisher>Melbourne, Australia: Blackwell Publishing Asia</publisher><subject>Acute Disease ; acute hepatitis ; AKT protein ; Alanine transaminase ; Alanine Transaminase - blood ; Animals ; Antibodies ; Apoptosis ; Apoptosis - drug effects ; Apoptosis Regulatory Proteins - metabolism ; Bcl-x protein ; Biological and medical sciences ; Caspase-3 ; Cell Line ; Disease Models, Animal ; Endothelial cells ; Endothelial Cells - drug effects ; Endothelial Cells - metabolism ; Endothelial Cells - pathology ; fas Receptor - immunology ; Gastroenterology. Liver. Pancreas. Abdomen ; Hemorrhage ; Hepatitis ; Hepatitis - blood ; Hepatitis - immunology ; Hepatitis - pathology ; Hepatitis - prevention & control ; hepatocyte ; Hepatocytes ; Hepatocytes - drug effects ; Hepatocytes - metabolism ; Hepatocytes - pathology ; In Situ Nick-End Labeling ; Liver ; Liver. Biliary tract. Portal circulation. Exocrine pancreas ; Male ; Medical sciences ; Mice ; Mice, Inbred C57BL ; Necrosis ; Other diseases. Semiology ; Phosphorylation ; Platelet Count ; Platelets ; Polyethylene Glycols ; Recombinant Proteins ; Staurosporine ; Staurosporine - pharmacology ; Thrombocytopenia - blood ; Thrombocytopenia - chemically induced ; Thrombocytopenia - pathology ; thrombocytosis ; Thrombocytosis - blood ; Thrombocytosis - chemically induced ; Thrombocytosis - pathology ; Thrombopoiesis ; Thrombopoietin ; Time Factors</subject><ispartof>Journal of gastroenterology and hepatology, 2011-02, Vol.26 (2), p.348-355</ispartof><rights>2011 Journal of Gastroenterology and Hepatology Foundation and Blackwell Publishing Asia Pty Ltd</rights><rights>2015 INIST-CNRS</rights><rights>2011 Journal of Gastroenterology and Hepatology Foundation and Blackwell Publishing Asia Pty Ltd.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5854-9335ee104f01c48faea2532c8585474f13d4c5030ce3148751e0dc767cc1218b3</citedby><cites>FETCH-LOGICAL-c5854-9335ee104f01c48faea2532c8585474f13d4c5030ce3148751e0dc767cc1218b3</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.1440-1746.2010.06334.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1440-1746.2010.06334.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,777,781,1412,27905,27906,45555,45556</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=23811633$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21261726$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hisakura, Katsuji</creatorcontrib><creatorcontrib>Murata, Soichiro</creatorcontrib><creatorcontrib>Takahashi, Kazuhiro</creatorcontrib><creatorcontrib>Matsuo, Ryota</creatorcontrib><creatorcontrib>Pak, Sugiru</creatorcontrib><creatorcontrib>Ikeda, Naoya</creatorcontrib><creatorcontrib>Kawasaki, Takuya</creatorcontrib><creatorcontrib>Kohno, Keisuke</creatorcontrib><creatorcontrib>Myronovych, Andriy</creatorcontrib><creatorcontrib>Nakano, Yoritaka</creatorcontrib><creatorcontrib>Ikeda, Osamu</creatorcontrib><creatorcontrib>Watanabe, Motonobu</creatorcontrib><creatorcontrib>Ohkohchi, Nobuhiro</creatorcontrib><title>Platelets prevent acute hepatitis induced by anti-fas antibody</title><title>Journal of gastroenterology and hepatology</title><addtitle>J Gastroenterol Hepatol</addtitle><description>Background and Aim: Platelets provide many functions in the body, especially to the liver. The purpose of this study is to investigate the effect of thrombocytosis with acute hepatitis induced by anti‐Fas antibody and its mechanism.
Methods: Acute hepatitis was induced by administration of anti‐Fas antibody in normal and thrombocytotic C57BL6J mice. For thrombocytosis, thrombopoietin; PEG‐rHuMGDF was injected 5 days before and just prior to administration of anti‐Fas antibody. To investigate the mechanisms, hepatocyte cell line (AML12) and sinusoidal endothelial cell line (M1) were induced apoptosis by staurosporine. They were cultured with platelets or thrombopoietin. Examination items were as follows: platelet number, alanine aminotransferase (ALT), histological findings, TUNEL (TdT‐mediated dUTP‐biotin Nick End Labeling) staining, and the expression of proteins associated with apoptosis in vivo and in vitro.
Results: Platelets were significantly increased in the thrombocytotic group (P < 0.01). Serum ALT levels were significantly reduced by thrombocytosis at 6, 24 and 72 h after the administration (P < 0.05). In histological findings, hemorrhagic necrosis was observed in the normal group, but not observed in the thrombocytotic group. TUNEL‐positive hepatocytes were reduced and the expression of cleaved caspase‐3 was significantly decreased in the thrombocytotic group. The phosphorylation of Akt, the increment of Bcl‐xL and the decrease of cleaved caspase‐3 were observed in AML12 cells cultured with platelets, but were not observed cultured with thrombopoietin. Platelets and thrombopoietin had no anti‐apoptotic effect on M1 cells.
Conclusion: Increase of platelets has a preventative effect against acute hepatitis induced by the anti‐Fas antibody. It is suggested that platelets have a direct protective effect against apoptosis of hepatocytes.</description><subject>Acute Disease</subject><subject>acute hepatitis</subject><subject>AKT protein</subject><subject>Alanine transaminase</subject><subject>Alanine Transaminase - blood</subject><subject>Animals</subject><subject>Antibodies</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Apoptosis Regulatory Proteins - metabolism</subject><subject>Bcl-x protein</subject><subject>Biological and medical sciences</subject><subject>Caspase-3</subject><subject>Cell Line</subject><subject>Disease Models, Animal</subject><subject>Endothelial cells</subject><subject>Endothelial Cells - drug effects</subject><subject>Endothelial Cells - metabolism</subject><subject>Endothelial Cells - pathology</subject><subject>fas Receptor - immunology</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Hemorrhage</subject><subject>Hepatitis</subject><subject>Hepatitis - blood</subject><subject>Hepatitis - immunology</subject><subject>Hepatitis - pathology</subject><subject>Hepatitis - prevention & control</subject><subject>hepatocyte</subject><subject>Hepatocytes</subject><subject>Hepatocytes - drug effects</subject><subject>Hepatocytes - metabolism</subject><subject>Hepatocytes - pathology</subject><subject>In Situ Nick-End Labeling</subject><subject>Liver</subject><subject>Liver. Biliary tract. Portal circulation. Exocrine pancreas</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Necrosis</subject><subject>Other diseases. Semiology</subject><subject>Phosphorylation</subject><subject>Platelet Count</subject><subject>Platelets</subject><subject>Polyethylene Glycols</subject><subject>Recombinant Proteins</subject><subject>Staurosporine</subject><subject>Staurosporine - pharmacology</subject><subject>Thrombocytopenia - blood</subject><subject>Thrombocytopenia - chemically induced</subject><subject>Thrombocytopenia - pathology</subject><subject>thrombocytosis</subject><subject>Thrombocytosis - blood</subject><subject>Thrombocytosis - chemically induced</subject><subject>Thrombocytosis - pathology</subject><subject>Thrombopoiesis</subject><subject>Thrombopoietin</subject><subject>Time Factors</subject><issn>0815-9319</issn><issn>1440-1746</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkE1vEzEQhi1ERUPhL6C9IHrZdMYfa-cAEqpKSqmAQwGJi-V4Z4XDZhPWXkj-Pd4mhBvCF488zzsePYwVCFPM52I5RSmhRC2rKYf8CpUQcrp9wCbHxkM2AYOqnAmcnbLHMS4BQIJWj9gpR16h5tWEvfrYukQtpVhsevpJXSqcHxIV32jjUkghFqGrB091sdgVrkuhbFy8LxbreveEnTSujfT0cJ-xT2-u7i6vy9sP87eXr29Lr4ySeQehiBBkA-ilaRw5rgT3Zuxq2aCopVcgwJNAabRCgtrrSnuPHM1CnLEX-7mbfv1joJjsKkRPbes6Wg_RmjxFKG10Js__SSJwMEpxgxk1e9T36xh7auymDyvX7zJkR892aUeddtRpR8_23rPd5uizwy_DYkX1MfhHbAaeHwAXvWub3nU-xL-cMIh5VuZe7rlfoaXdfy9gb-bXY5Xz5T4fYqLtMe_677bSQiv75f3cwuzu3Q1-_WyN-A3QVqVw</recordid><startdate>201102</startdate><enddate>201102</enddate><creator>Hisakura, Katsuji</creator><creator>Murata, Soichiro</creator><creator>Takahashi, Kazuhiro</creator><creator>Matsuo, Ryota</creator><creator>Pak, Sugiru</creator><creator>Ikeda, Naoya</creator><creator>Kawasaki, Takuya</creator><creator>Kohno, Keisuke</creator><creator>Myronovych, Andriy</creator><creator>Nakano, Yoritaka</creator><creator>Ikeda, Osamu</creator><creator>Watanabe, Motonobu</creator><creator>Ohkohchi, Nobuhiro</creator><general>Blackwell Publishing Asia</general><general>Wiley-Blackwell</general><scope>BSCLL</scope><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>7U9</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>201102</creationdate><title>Platelets prevent acute hepatitis induced by anti-fas antibody</title><author>Hisakura, Katsuji ; Murata, Soichiro ; Takahashi, Kazuhiro ; Matsuo, Ryota ; Pak, Sugiru ; Ikeda, Naoya ; Kawasaki, Takuya ; Kohno, Keisuke ; Myronovych, Andriy ; Nakano, Yoritaka ; Ikeda, Osamu ; Watanabe, Motonobu ; Ohkohchi, Nobuhiro</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5854-9335ee104f01c48faea2532c8585474f13d4c5030ce3148751e0dc767cc1218b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Acute Disease</topic><topic>acute hepatitis</topic><topic>AKT protein</topic><topic>Alanine transaminase</topic><topic>Alanine Transaminase - blood</topic><topic>Animals</topic><topic>Antibodies</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Apoptosis Regulatory Proteins - metabolism</topic><topic>Bcl-x protein</topic><topic>Biological and medical sciences</topic><topic>Caspase-3</topic><topic>Cell Line</topic><topic>Disease Models, Animal</topic><topic>Endothelial cells</topic><topic>Endothelial Cells - drug effects</topic><topic>Endothelial Cells - metabolism</topic><topic>Endothelial Cells - pathology</topic><topic>fas Receptor - immunology</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Hemorrhage</topic><topic>Hepatitis</topic><topic>Hepatitis - blood</topic><topic>Hepatitis - immunology</topic><topic>Hepatitis - pathology</topic><topic>Hepatitis - prevention & control</topic><topic>hepatocyte</topic><topic>Hepatocytes</topic><topic>Hepatocytes - drug effects</topic><topic>Hepatocytes - metabolism</topic><topic>Hepatocytes - pathology</topic><topic>In Situ Nick-End Labeling</topic><topic>Liver</topic><topic>Liver. Biliary tract. Portal circulation. Exocrine pancreas</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Necrosis</topic><topic>Other diseases. Semiology</topic><topic>Phosphorylation</topic><topic>Platelet Count</topic><topic>Platelets</topic><topic>Polyethylene Glycols</topic><topic>Recombinant Proteins</topic><topic>Staurosporine</topic><topic>Staurosporine - pharmacology</topic><topic>Thrombocytopenia - blood</topic><topic>Thrombocytopenia - chemically induced</topic><topic>Thrombocytopenia - pathology</topic><topic>thrombocytosis</topic><topic>Thrombocytosis - blood</topic><topic>Thrombocytosis - chemically induced</topic><topic>Thrombocytosis - pathology</topic><topic>Thrombopoiesis</topic><topic>Thrombopoietin</topic><topic>Time Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hisakura, Katsuji</creatorcontrib><creatorcontrib>Murata, Soichiro</creatorcontrib><creatorcontrib>Takahashi, Kazuhiro</creatorcontrib><creatorcontrib>Matsuo, Ryota</creatorcontrib><creatorcontrib>Pak, Sugiru</creatorcontrib><creatorcontrib>Ikeda, Naoya</creatorcontrib><creatorcontrib>Kawasaki, Takuya</creatorcontrib><creatorcontrib>Kohno, Keisuke</creatorcontrib><creatorcontrib>Myronovych, Andriy</creatorcontrib><creatorcontrib>Nakano, Yoritaka</creatorcontrib><creatorcontrib>Ikeda, Osamu</creatorcontrib><creatorcontrib>Watanabe, Motonobu</creatorcontrib><creatorcontrib>Ohkohchi, Nobuhiro</creatorcontrib><collection>Istex</collection><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>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of gastroenterology and hepatology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hisakura, Katsuji</au><au>Murata, Soichiro</au><au>Takahashi, Kazuhiro</au><au>Matsuo, Ryota</au><au>Pak, Sugiru</au><au>Ikeda, Naoya</au><au>Kawasaki, Takuya</au><au>Kohno, Keisuke</au><au>Myronovych, Andriy</au><au>Nakano, Yoritaka</au><au>Ikeda, Osamu</au><au>Watanabe, Motonobu</au><au>Ohkohchi, Nobuhiro</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Platelets prevent acute hepatitis induced by anti-fas antibody</atitle><jtitle>Journal of gastroenterology and hepatology</jtitle><addtitle>J Gastroenterol Hepatol</addtitle><date>2011-02</date><risdate>2011</risdate><volume>26</volume><issue>2</issue><spage>348</spage><epage>355</epage><pages>348-355</pages><issn>0815-9319</issn><eissn>1440-1746</eissn><abstract>Background and Aim: Platelets provide many functions in the body, especially to the liver. The purpose of this study is to investigate the effect of thrombocytosis with acute hepatitis induced by anti‐Fas antibody and its mechanism.
Methods: Acute hepatitis was induced by administration of anti‐Fas antibody in normal and thrombocytotic C57BL6J mice. For thrombocytosis, thrombopoietin; PEG‐rHuMGDF was injected 5 days before and just prior to administration of anti‐Fas antibody. To investigate the mechanisms, hepatocyte cell line (AML12) and sinusoidal endothelial cell line (M1) were induced apoptosis by staurosporine. They were cultured with platelets or thrombopoietin. Examination items were as follows: platelet number, alanine aminotransferase (ALT), histological findings, TUNEL (TdT‐mediated dUTP‐biotin Nick End Labeling) staining, and the expression of proteins associated with apoptosis in vivo and in vitro.
Results: Platelets were significantly increased in the thrombocytotic group (P < 0.01). Serum ALT levels were significantly reduced by thrombocytosis at 6, 24 and 72 h after the administration (P < 0.05). In histological findings, hemorrhagic necrosis was observed in the normal group, but not observed in the thrombocytotic group. TUNEL‐positive hepatocytes were reduced and the expression of cleaved caspase‐3 was significantly decreased in the thrombocytotic group. The phosphorylation of Akt, the increment of Bcl‐xL and the decrease of cleaved caspase‐3 were observed in AML12 cells cultured with platelets, but were not observed cultured with thrombopoietin. Platelets and thrombopoietin had no anti‐apoptotic effect on M1 cells.
Conclusion: Increase of platelets has a preventative effect against acute hepatitis induced by the anti‐Fas antibody. It is suggested that platelets have a direct protective effect against apoptosis of hepatocytes.</abstract><cop>Melbourne, Australia</cop><pub>Blackwell Publishing Asia</pub><pmid>21261726</pmid><doi>10.1111/j.1440-1746.2010.06334.x</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Acute Disease acute hepatitis AKT protein Alanine transaminase Alanine Transaminase - blood Animals Antibodies Apoptosis Apoptosis - drug effects Apoptosis Regulatory Proteins - metabolism Bcl-x protein Biological and medical sciences Caspase-3 Cell Line Disease Models, Animal Endothelial cells Endothelial Cells - drug effects Endothelial Cells - metabolism Endothelial Cells - pathology fas Receptor - immunology Gastroenterology. Liver. Pancreas. Abdomen Hemorrhage Hepatitis Hepatitis - blood Hepatitis - immunology Hepatitis - pathology Hepatitis - prevention & control hepatocyte Hepatocytes Hepatocytes - drug effects Hepatocytes - metabolism Hepatocytes - pathology In Situ Nick-End Labeling Liver Liver. Biliary tract. Portal circulation. Exocrine pancreas Male Medical sciences Mice Mice, Inbred C57BL Necrosis Other diseases. Semiology Phosphorylation Platelet Count Platelets Polyethylene Glycols Recombinant Proteins Staurosporine Staurosporine - pharmacology Thrombocytopenia - blood Thrombocytopenia - chemically induced Thrombocytopenia - pathology thrombocytosis Thrombocytosis - blood Thrombocytosis - chemically induced Thrombocytosis - pathology Thrombopoiesis Thrombopoietin Time Factors |
| title | Platelets prevent acute hepatitis induced by anti-fas antibody |
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