Modulation of no synthesis by plaferon LB in liver
Nitric oxide (NO) is a free radical involved in the regulation of many physiological processes. NO exerts important effects on liver in health and diseases. In the present study, we attempted to evaluate the influence of plaferon LB on the liver injury in two experimental models: immune-mediated and...
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Veröffentlicht in: | Georgian medical news 2006-04 (133), p.102-104 |
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description | Nitric oxide (NO) is a free radical involved in the regulation of many physiological processes. NO exerts important effects on liver in health and diseases. In the present study, we attempted to evaluate the influence of plaferon LB on the liver injury in two experimental models: immune-mediated and mechanical (traumatic shock) liver damage models. The results of our study demonstrated that plaferon LB decreased levels of NO in traumatic shock, but enhanced NO expression on con-A induced hepatitis. Furthermore, plaferon LB inhibited development of metabolic changes in liver tissue and facilitated restoration of hepatocyte function and structure of the tissue. Thus, our data revealed that plaferon LB was a powerful regulator of NO levels in experimental liver injury. Further investigations are needed to determine pro- and anti-apoptotic properties of plaferon LB in the liver. |
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NO exerts important effects on liver in health and diseases. In the present study, we attempted to evaluate the influence of plaferon LB on the liver injury in two experimental models: immune-mediated and mechanical (traumatic shock) liver damage models. The results of our study demonstrated that plaferon LB decreased levels of NO in traumatic shock, but enhanced NO expression on con-A induced hepatitis. Furthermore, plaferon LB inhibited development of metabolic changes in liver tissue and facilitated restoration of hepatocyte function and structure of the tissue. Thus, our data revealed that plaferon LB was a powerful regulator of NO levels in experimental liver injury. Further investigations are needed to determine pro- and anti-apoptotic properties of plaferon LB in the liver.</description><identifier>ISSN: 1512-0112</identifier><identifier>PMID: 16705244</identifier><language>eng</language><publisher>Georgia (Republic)</publisher><subject>Animals ; Hypoxia, Brain - etiology ; Hypoxia, Brain - prevention & control ; Liver - injuries ; Liver - metabolism ; Mice ; Neuropeptides - pharmacology ; Nitric Oxide - metabolism ; Rats ; Shock, Traumatic - complications ; Shock, Traumatic - drug therapy ; Wounds and Injuries - drug therapy</subject><ispartof>Georgian medical news, 2006-04 (133), p.102-104</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,777,781</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16705244$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sirbiladze, G</creatorcontrib><creatorcontrib>Kikodze, N</creatorcontrib><creatorcontrib>Iobadze, M</creatorcontrib><creatorcontrib>Chikovani, T</creatorcontrib><creatorcontrib>Datunashvili, I</creatorcontrib><title>Modulation of no synthesis by plaferon LB in liver</title><title>Georgian medical news</title><addtitle>Georgian Med News</addtitle><description>Nitric oxide (NO) is a free radical involved in the regulation of many physiological processes. NO exerts important effects on liver in health and diseases. In the present study, we attempted to evaluate the influence of plaferon LB on the liver injury in two experimental models: immune-mediated and mechanical (traumatic shock) liver damage models. The results of our study demonstrated that plaferon LB decreased levels of NO in traumatic shock, but enhanced NO expression on con-A induced hepatitis. Furthermore, plaferon LB inhibited development of metabolic changes in liver tissue and facilitated restoration of hepatocyte function and structure of the tissue. Thus, our data revealed that plaferon LB was a powerful regulator of NO levels in experimental liver injury. Further investigations are needed to determine pro- and anti-apoptotic properties of plaferon LB in the liver.</description><subject>Animals</subject><subject>Hypoxia, Brain - etiology</subject><subject>Hypoxia, Brain - prevention & control</subject><subject>Liver - injuries</subject><subject>Liver - metabolism</subject><subject>Mice</subject><subject>Neuropeptides - pharmacology</subject><subject>Nitric Oxide - metabolism</subject><subject>Rats</subject><subject>Shock, Traumatic - complications</subject><subject>Shock, Traumatic - drug therapy</subject><subject>Wounds and Injuries - drug therapy</subject><issn>1512-0112</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo1T8tKxDAUzUJxhnF-QbJyV8j7sdTBF1Tc6LokTYKRtKlNK_TvDTiezeFyHtxzAfaYY9IgjMkOHEv5QhWcCYXZFdhhIREnjO0Bec1uTWaJeYQ5wDHDso3Lpy-xQLvBKZng56q19zCOMMUfP1-Dy2BS8cczH8DH48P76blp355eTndtM2HClqZHwVjWUyUNsbRHhBBvnQz17onj2glhrbJBcx4UpoxKpVnwWNXHNAqaHsDtX-805-_Vl6UbYul9Smb0eS2dkLpGtKjGm7NxtYN33TTHwcxb97-S_gLDJEyI</recordid><startdate>200604</startdate><enddate>200604</enddate><creator>Sirbiladze, G</creator><creator>Kikodze, N</creator><creator>Iobadze, M</creator><creator>Chikovani, T</creator><creator>Datunashvili, I</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>200604</creationdate><title>Modulation of no synthesis by plaferon LB in liver</title><author>Sirbiladze, G ; Kikodze, N ; Iobadze, M ; Chikovani, T ; Datunashvili, I</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p124t-c0fab4c387a2b3c0222ebd7f87ac2d59d66bb8bf955f813437894fe1852490f93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Animals</topic><topic>Hypoxia, Brain - etiology</topic><topic>Hypoxia, Brain - prevention & control</topic><topic>Liver - injuries</topic><topic>Liver - metabolism</topic><topic>Mice</topic><topic>Neuropeptides - pharmacology</topic><topic>Nitric Oxide - metabolism</topic><topic>Rats</topic><topic>Shock, Traumatic - complications</topic><topic>Shock, Traumatic - drug therapy</topic><topic>Wounds and Injuries - drug therapy</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sirbiladze, G</creatorcontrib><creatorcontrib>Kikodze, N</creatorcontrib><creatorcontrib>Iobadze, M</creatorcontrib><creatorcontrib>Chikovani, T</creatorcontrib><creatorcontrib>Datunashvili, I</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>Georgian medical news</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sirbiladze, G</au><au>Kikodze, N</au><au>Iobadze, M</au><au>Chikovani, T</au><au>Datunashvili, I</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Modulation of no synthesis by plaferon LB in liver</atitle><jtitle>Georgian medical news</jtitle><addtitle>Georgian Med News</addtitle><date>2006-04</date><risdate>2006</risdate><issue>133</issue><spage>102</spage><epage>104</epage><pages>102-104</pages><issn>1512-0112</issn><abstract>Nitric oxide (NO) is a free radical involved in the regulation of many physiological processes. NO exerts important effects on liver in health and diseases. In the present study, we attempted to evaluate the influence of plaferon LB on the liver injury in two experimental models: immune-mediated and mechanical (traumatic shock) liver damage models. The results of our study demonstrated that plaferon LB decreased levels of NO in traumatic shock, but enhanced NO expression on con-A induced hepatitis. Furthermore, plaferon LB inhibited development of metabolic changes in liver tissue and facilitated restoration of hepatocyte function and structure of the tissue. Thus, our data revealed that plaferon LB was a powerful regulator of NO levels in experimental liver injury. Further investigations are needed to determine pro- and anti-apoptotic properties of plaferon LB in the liver.</abstract><cop>Georgia (Republic)</cop><pmid>16705244</pmid><tpages>3</tpages></addata></record> |
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subjects | Animals Hypoxia, Brain - etiology Hypoxia, Brain - prevention & control Liver - injuries Liver - metabolism Mice Neuropeptides - pharmacology Nitric Oxide - metabolism Rats Shock, Traumatic - complications Shock, Traumatic - drug therapy Wounds and Injuries - drug therapy |
title | Modulation of no synthesis by plaferon LB in liver |
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