Protective Effect of Ulinastatin against Liver Injury Caused by Ischemia-Reperfusion in Rats
The effects of ulinastatin (ULN), a human urinary pro tease inhibitor, on liver injury caused by ischemia-reperfusion were studied in rats. In the liver ischemia-reperfusion model, ULN suppressed the elevation of serum transaminase levels and tissue lipid peroxide levels in the liver. ULN did not ex...
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| Veröffentlicht in: | Japanese Journal of Pharmacology 1992, Vol.60 (3), p.239-245 |
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| creator | Yoshikuni, Kudo Toru, Egashira Yasumitsu, Yamanaka |
| description | The effects of ulinastatin (ULN), a human urinary pro tease inhibitor, on liver injury caused by ischemia-reperfusion were studied in rats. In the liver ischemia-reperfusion model, ULN suppressed the elevation of serum transaminase levels and tissue lipid peroxide levels in the liver. ULN did not exhibit a radical-trapping action on the superoxide and hydroxyl radicals as measured by electron spin resonance (ESR). ULN suppressed formylmethionyl-leucyl-phenylalanine (FMLP) and phorbol myristate acetate (PMA)-induced superoxide production from polymorphonuclear leukocytes (PMNs) as measured by the cytochrome c assay. ULN did not inhibit either xanthine oxidase (XO) activity or the conversion of xanthine dehydrogenase (XDH) to XO during the ischemic period. ULN also strongly protected against the hypotonic hemolysis of rat erythrocytes. These results suggest that ULN’s membrane stabilizing action and suppressive effect against PMNs superoxide production might be attributed to its suppressive effect on the liver’s lipid peroxidation caused by ischemia-reperfusion. |
| doi_str_mv | 10.1016/S0021-5198(19)32414-X |
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In the liver ischemia-reperfusion model, ULN suppressed the elevation of serum transaminase levels and tissue lipid peroxide levels in the liver. ULN did not exhibit a radical-trapping action on the superoxide and hydroxyl radicals as measured by electron spin resonance (ESR). ULN suppressed formylmethionyl-leucyl-phenylalanine (FMLP) and phorbol myristate acetate (PMA)-induced superoxide production from polymorphonuclear leukocytes (PMNs) as measured by the cytochrome c assay. ULN did not inhibit either xanthine oxidase (XO) activity or the conversion of xanthine dehydrogenase (XDH) to XO during the ischemic period. ULN also strongly protected against the hypotonic hemolysis of rat erythrocytes. These results suggest that ULN’s membrane stabilizing action and suppressive effect against PMNs superoxide production might be attributed to its suppressive effect on the liver’s lipid peroxidation caused by ischemia-reperfusion.</description><identifier>ISSN: 0021-5198</identifier><identifier>EISSN: 1347-3506</identifier><identifier>DOI: 10.1016/S0021-5198(19)32414-X</identifier><identifier>PMID: 1337129</identifier><identifier>CODEN: JJPAAZ</identifier><language>eng</language><publisher>Kyoto: The Japanese Pharmacological Society</publisher><subject>Animals ; Antianginal agents. Coronary vasodilator agents ; Biological and medical sciences ; Cardiovascular system ; Enzymes - blood ; Erythrocyte Membrane - drug effects ; Free Radicals ; Glycoproteins - therapeutic use ; Ischemia - physiopathology ; Ischemia-reperfusion ; Lipid peroxidation ; Lipid Peroxides - metabolism ; Liver - injuries ; Liver Circulation - drug effects ; Male ; Medical sciences ; Membrane stabilization ; Neutrophils - drug effects ; Neutrophils - enzymology ; Pharmacology. Drug treatments ; Polymorphonuclear leukocyte ; Protease Inhibitors - therapeutic use ; Rats ; Rats, Wistar ; Reperfusion Injury - enzymology ; Reperfusion Injury - prevention & control ; Superoxides - metabolism ; Trypsin Inhibitors - therapeutic use ; Ulinastatin ; Xanthine Oxidase - metabolism</subject><ispartof>Japanese Journal of Pharmacology, 1992, Vol.60 (3), p.239-245</ispartof><rights>1992 Elsevier B.V.</rights><rights>1993 INIST-CNRS</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c390x-add3e9a13ea908d02e754f877fd0c5322b0fce14bab748ad9006a9d5da9a1ce13</citedby><cites>FETCH-LOGICAL-c390x-add3e9a13ea908d02e754f877fd0c5322b0fce14bab748ad9006a9d5da9a1ce13</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,4010,27900,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=4569498$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/1337129$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yoshikuni, Kudo</creatorcontrib><creatorcontrib>Toru, Egashira</creatorcontrib><creatorcontrib>Yasumitsu, Yamanaka</creatorcontrib><creatorcontrib>Department of Pharmacology</creatorcontrib><creatorcontrib>Oita Medical University</creatorcontrib><title>Protective Effect of Ulinastatin against Liver Injury Caused by Ischemia-Reperfusion in Rats</title><title>Japanese Journal of Pharmacology</title><addtitle>Jpn J Pharmacol</addtitle><description>The effects of ulinastatin (ULN), a human urinary pro tease inhibitor, on liver injury caused by ischemia-reperfusion were studied in rats. In the liver ischemia-reperfusion model, ULN suppressed the elevation of serum transaminase levels and tissue lipid peroxide levels in the liver. ULN did not exhibit a radical-trapping action on the superoxide and hydroxyl radicals as measured by electron spin resonance (ESR). ULN suppressed formylmethionyl-leucyl-phenylalanine (FMLP) and phorbol myristate acetate (PMA)-induced superoxide production from polymorphonuclear leukocytes (PMNs) as measured by the cytochrome c assay. ULN did not inhibit either xanthine oxidase (XO) activity or the conversion of xanthine dehydrogenase (XDH) to XO during the ischemic period. ULN also strongly protected against the hypotonic hemolysis of rat erythrocytes. These results suggest that ULN’s membrane stabilizing action and suppressive effect against PMNs superoxide production might be attributed to its suppressive effect on the liver’s lipid peroxidation caused by ischemia-reperfusion.</description><subject>Animals</subject><subject>Antianginal agents. Coronary vasodilator agents</subject><subject>Biological and medical sciences</subject><subject>Cardiovascular system</subject><subject>Enzymes - blood</subject><subject>Erythrocyte Membrane - drug effects</subject><subject>Free Radicals</subject><subject>Glycoproteins - therapeutic use</subject><subject>Ischemia - physiopathology</subject><subject>Ischemia-reperfusion</subject><subject>Lipid peroxidation</subject><subject>Lipid Peroxides - metabolism</subject><subject>Liver - injuries</subject><subject>Liver Circulation - drug effects</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Membrane stabilization</subject><subject>Neutrophils - drug effects</subject><subject>Neutrophils - enzymology</subject><subject>Pharmacology. Drug treatments</subject><subject>Polymorphonuclear leukocyte</subject><subject>Protease Inhibitors - therapeutic use</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Reperfusion Injury - enzymology</subject><subject>Reperfusion Injury - prevention & control</subject><subject>Superoxides - metabolism</subject><subject>Trypsin Inhibitors - therapeutic use</subject><subject>Ulinastatin</subject><subject>Xanthine Oxidase - metabolism</subject><issn>0021-5198</issn><issn>1347-3506</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1992</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkV1rFDEUhoModa3-hEIuRPRiNJkkM5MrkaXVhQWlWuiFEDL50AyzyTaZKe6_92xnqZfe5IPzvu_JeYLQBSXvKaHNh--E1LQSVHZvqXzHak55dfsErSjjbcUEaZ6i1aPkOXpRygDXjlB-hs4oYy2t5Qr9_JbT5MwU7h2-9B5OOHl8M4aoy6SnELH-pUMsE96CJONNHOZ8wGs9F2dxf8CbYn67XdDVtdu77OcSUsRgu9ZTeYmeeT0W9-q0n6Obq8sf6y_V9uvnzfrTtjJMkj-VtpY5qSlzWpLOktq1gvuubb0lRrC67ok3jvJe9y3vtJWENFpaYTWYoMDO0Zsld5_T3ezKpHahGDeOOro0F9UyQWsqOhCKRWhyKiU7r_Y57HQ-KErUkap6oKqOyBSV6oGqugXfxanB3O-c_edaMEL99amui9GjzzqaUB5lXDSSy2P7q0UGGQF0KQJnp4Y05wh8lPHNMKT9CK1lrWBKQpgi8DRSMwkLhzGIaDgEfVyCHFC9Dy6rYoKLBmIzfKGyKfxnor9rhKrU</recordid><startdate>1992</startdate><enddate>1992</enddate><creator>Yoshikuni, Kudo</creator><creator>Toru, Egashira</creator><creator>Yasumitsu, Yamanaka</creator><general>The Japanese Pharmacological Society</general><general>Japanese Pharmacological Society</general><scope>6I.</scope><scope>AAFTH</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>7X8</scope></search><sort><creationdate>1992</creationdate><title>Protective Effect of Ulinastatin against Liver Injury Caused by Ischemia-Reperfusion in Rats</title><author>Yoshikuni, Kudo ; Toru, Egashira ; Yasumitsu, Yamanaka</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c390x-add3e9a13ea908d02e754f877fd0c5322b0fce14bab748ad9006a9d5da9a1ce13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1992</creationdate><topic>Animals</topic><topic>Antianginal agents. Coronary vasodilator agents</topic><topic>Biological and medical sciences</topic><topic>Cardiovascular system</topic><topic>Enzymes - blood</topic><topic>Erythrocyte Membrane - drug effects</topic><topic>Free Radicals</topic><topic>Glycoproteins - therapeutic use</topic><topic>Ischemia - physiopathology</topic><topic>Ischemia-reperfusion</topic><topic>Lipid peroxidation</topic><topic>Lipid Peroxides - metabolism</topic><topic>Liver - injuries</topic><topic>Liver Circulation - drug effects</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Membrane stabilization</topic><topic>Neutrophils - drug effects</topic><topic>Neutrophils - enzymology</topic><topic>Pharmacology. Drug treatments</topic><topic>Polymorphonuclear leukocyte</topic><topic>Protease Inhibitors - therapeutic use</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Reperfusion Injury - enzymology</topic><topic>Reperfusion Injury - prevention & control</topic><topic>Superoxides - metabolism</topic><topic>Trypsin Inhibitors - therapeutic use</topic><topic>Ulinastatin</topic><topic>Xanthine Oxidase - metabolism</topic><toplevel>online_resources</toplevel><creatorcontrib>Yoshikuni, Kudo</creatorcontrib><creatorcontrib>Toru, Egashira</creatorcontrib><creatorcontrib>Yasumitsu, Yamanaka</creatorcontrib><creatorcontrib>Department of Pharmacology</creatorcontrib><creatorcontrib>Oita Medical University</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</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>MEDLINE - Academic</collection><jtitle>Japanese Journal of Pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yoshikuni, Kudo</au><au>Toru, Egashira</au><au>Yasumitsu, Yamanaka</au><aucorp>Department of Pharmacology</aucorp><aucorp>Oita Medical University</aucorp><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Protective Effect of Ulinastatin against Liver Injury Caused by Ischemia-Reperfusion in Rats</atitle><jtitle>Japanese Journal of Pharmacology</jtitle><addtitle>Jpn J Pharmacol</addtitle><date>1992</date><risdate>1992</risdate><volume>60</volume><issue>3</issue><spage>239</spage><epage>245</epage><pages>239-245</pages><issn>0021-5198</issn><eissn>1347-3506</eissn><coden>JJPAAZ</coden><abstract>The effects of ulinastatin (ULN), a human urinary pro tease inhibitor, on liver injury caused by ischemia-reperfusion were studied in rats. In the liver ischemia-reperfusion model, ULN suppressed the elevation of serum transaminase levels and tissue lipid peroxide levels in the liver. ULN did not exhibit a radical-trapping action on the superoxide and hydroxyl radicals as measured by electron spin resonance (ESR). ULN suppressed formylmethionyl-leucyl-phenylalanine (FMLP) and phorbol myristate acetate (PMA)-induced superoxide production from polymorphonuclear leukocytes (PMNs) as measured by the cytochrome c assay. ULN did not inhibit either xanthine oxidase (XO) activity or the conversion of xanthine dehydrogenase (XDH) to XO during the ischemic period. ULN also strongly protected against the hypotonic hemolysis of rat erythrocytes. These results suggest that ULN’s membrane stabilizing action and suppressive effect against PMNs superoxide production might be attributed to its suppressive effect on the liver’s lipid peroxidation caused by ischemia-reperfusion.</abstract><cop>Kyoto</cop><pub>The Japanese Pharmacological Society</pub><pmid>1337129</pmid><doi>10.1016/S0021-5198(19)32414-X</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| source | J-STAGE Free; MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Free Full-Text Journals in Chemistry |
| subjects | Animals Antianginal agents. Coronary vasodilator agents Biological and medical sciences Cardiovascular system Enzymes - blood Erythrocyte Membrane - drug effects Free Radicals Glycoproteins - therapeutic use Ischemia - physiopathology Ischemia-reperfusion Lipid peroxidation Lipid Peroxides - metabolism Liver - injuries Liver Circulation - drug effects Male Medical sciences Membrane stabilization Neutrophils - drug effects Neutrophils - enzymology Pharmacology. Drug treatments Polymorphonuclear leukocyte Protease Inhibitors - therapeutic use Rats Rats, Wistar Reperfusion Injury - enzymology Reperfusion Injury - prevention & control Superoxides - metabolism Trypsin Inhibitors - therapeutic use Ulinastatin Xanthine Oxidase - metabolism |
| title | Protective Effect of Ulinastatin against Liver Injury Caused by Ischemia-Reperfusion in Rats |
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