Effects of globin digest and its active ingredient Trp-Thr-Gln-Arg on galactosamine/lipopolysaccharide-induced liver injury in ICR mice
We investigated the effects of globin digest (GD) and its active ingredient Trp-Thr-Gln-Arg (WTQR) on galactosamine/lipopolysaccharide (GalN/LPS)-induced liver injury in imprinting control region (ICR) mice. The effects of WTQR and GD on the liver injury were examined by measuring the survival rate,...
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| Veröffentlicht in: | Life sciences (1973) 2012-01, Vol.90 (5-6), p.190-199 |
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| creator | Sasakawa, Yuka Kominami, Akari Yamamoto, Kaori Nakaoka, Fumiko Nakamura, Miki Nakao, Mayumi Abe, Michiyo Fukuhama, Chizuko Kagawa, Kyoichi |
| description | We investigated the effects of globin digest (GD) and its active ingredient Trp-Thr-Gln-Arg (WTQR) on galactosamine/lipopolysaccharide (GalN/LPS)-induced liver injury in imprinting control region (ICR) mice.
The effects of WTQR and GD on the liver injury were examined by measuring the survival rate, serum aminotransferase activities, hepatic components, antioxidant enzyme activities, histopathological analysis, serum levels and hepatic gene expression of tumor necrosis factor-alpha (TNF-α), macrophage inflammatory protein-2 (MIP-2), and nitric oxide (NO) or inducible nitric oxide synthase (iNOS), and nuclear factor-kappa B (NF-κB) p65 content in GalN/LPS-treated ICR mice. RAW264 mouse macrophages were used to confirm the anti-inflammatory effects of WTQR and GD on the macrophages.
WTQR and GD increased the survival rate, suppressed the serum aminotransferase activities, serum levels and hepatic gene expression of TNF-α, MIP-2, and NO or iNOS, and nuclear NF-κB p65 content in GalN/LPS-treated mice; decreased the oxidized glutathione content, increased the superoxide dismutase activity, and decreased the histopathological grade values of the hepatocyte necrosis and lobular inflammation in GalN/LPS-injured liver; and suppressed the release levels and gene expression of TNF-α, MIP-2, and NO or iNOS, and nuclear NF-κB p65 content in LPS-stimulated RAW264 macrophages. WTQR and GD may improve the antioxidant defense system and inflammatory status in GalN/LPS-injured liver.
These findings indicate that WTQR and GD have hepatoprotective effects on GalN/LPS-induced liver injury in ICR mice. |
| doi_str_mv | 10.1016/j.lfs.2011.11.013 |
| format | Article |
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The effects of WTQR and GD on the liver injury were examined by measuring the survival rate, serum aminotransferase activities, hepatic components, antioxidant enzyme activities, histopathological analysis, serum levels and hepatic gene expression of tumor necrosis factor-alpha (TNF-α), macrophage inflammatory protein-2 (MIP-2), and nitric oxide (NO) or inducible nitric oxide synthase (iNOS), and nuclear factor-kappa B (NF-κB) p65 content in GalN/LPS-treated ICR mice. RAW264 mouse macrophages were used to confirm the anti-inflammatory effects of WTQR and GD on the macrophages.
WTQR and GD increased the survival rate, suppressed the serum aminotransferase activities, serum levels and hepatic gene expression of TNF-α, MIP-2, and NO or iNOS, and nuclear NF-κB p65 content in GalN/LPS-treated mice; decreased the oxidized glutathione content, increased the superoxide dismutase activity, and decreased the histopathological grade values of the hepatocyte necrosis and lobular inflammation in GalN/LPS-injured liver; and suppressed the release levels and gene expression of TNF-α, MIP-2, and NO or iNOS, and nuclear NF-κB p65 content in LPS-stimulated RAW264 macrophages. WTQR and GD may improve the antioxidant defense system and inflammatory status in GalN/LPS-injured liver.
These findings indicate that WTQR and GD have hepatoprotective effects on GalN/LPS-induced liver injury in ICR mice.</description><identifier>ISSN: 0024-3205</identifier><identifier>EISSN: 1879-0631</identifier><identifier>DOI: 10.1016/j.lfs.2011.11.013</identifier><identifier>PMID: 22154906</identifier><language>eng</language><publisher>Netherlands: Elsevier Inc</publisher><subject>active ingredients ; Analysis of Variance ; Animals ; anti-inflammatory activity ; antioxidants ; Antioxidants - metabolism ; blood serum ; Cell Line ; Chemical and Drug Induced Liver Injury - drug therapy ; Chemical and Drug Induced Liver Injury - immunology ; Chemical and Drug Induced Liver Injury - metabolism ; chemokine CXCL2 ; Chemokine CXCL2 - blood ; Chemokine CXCL2 - genetics ; enzyme activity ; Galactosamine ; Galactosamine - administration & dosage ; Galactosamine - adverse effects ; gene expression ; Globin digest ; Globins - administration & dosage ; Globins - chemistry ; glutathione ; Hepatocytes - drug effects ; Hepatocytes - metabolism ; hepatoprotective effect ; histopathology ; inducible nitric oxide synthase ; inflammation ; Lipopolysaccharide ; lipopolysaccharides ; Lipopolysaccharides - administration & dosage ; Lipopolysaccharides - adverse effects ; liver ; Liver - drug effects ; Liver - metabolism ; Liver - pathology ; Liver injury ; macrophages ; Macrophages - metabolism ; Male ; Mice ; Mice, Inbred ICR ; necrosis ; NF-kappa B - analysis ; NF-kappa B - metabolism ; nitric oxide ; Nitric Oxide - blood ; Nitric Oxide - metabolism ; Nitric Oxide Synthase Type II - genetics ; Nitric Oxide Synthase Type II - metabolism ; Oligopeptides - administration & dosage ; Peptide Fragments - administration & dosage ; Peptide Fragments - chemistry ; RAW264 ; superoxide dismutase ; Survival Rate ; Transaminases - blood ; transcription factor NF-kappa B ; Trp-Thr-Gln-Arg (WTQR) ; tumor necrosis factor-alpha ; Tumor Necrosis Factor-alpha - blood ; Tumor Necrosis Factor-alpha - genetics</subject><ispartof>Life sciences (1973), 2012-01, Vol.90 (5-6), p.190-199</ispartof><rights>2011 Elsevier Inc.</rights><rights>Copyright © 2011 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c291t-4785b69997117cdc6ac7edee520502521595d01c99d85543617c986178ebd1c93</citedby><cites>FETCH-LOGICAL-c291t-4785b69997117cdc6ac7edee520502521595d01c99d85543617c986178ebd1c93</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.lfs.2011.11.013$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3548,27923,27924,45994</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22154906$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sasakawa, Yuka</creatorcontrib><creatorcontrib>Kominami, Akari</creatorcontrib><creatorcontrib>Yamamoto, Kaori</creatorcontrib><creatorcontrib>Nakaoka, Fumiko</creatorcontrib><creatorcontrib>Nakamura, Miki</creatorcontrib><creatorcontrib>Nakao, Mayumi</creatorcontrib><creatorcontrib>Abe, Michiyo</creatorcontrib><creatorcontrib>Fukuhama, Chizuko</creatorcontrib><creatorcontrib>Kagawa, Kyoichi</creatorcontrib><title>Effects of globin digest and its active ingredient Trp-Thr-Gln-Arg on galactosamine/lipopolysaccharide-induced liver injury in ICR mice</title><title>Life sciences (1973)</title><addtitle>Life Sci</addtitle><description>We investigated the effects of globin digest (GD) and its active ingredient Trp-Thr-Gln-Arg (WTQR) on galactosamine/lipopolysaccharide (GalN/LPS)-induced liver injury in imprinting control region (ICR) mice.
The effects of WTQR and GD on the liver injury were examined by measuring the survival rate, serum aminotransferase activities, hepatic components, antioxidant enzyme activities, histopathological analysis, serum levels and hepatic gene expression of tumor necrosis factor-alpha (TNF-α), macrophage inflammatory protein-2 (MIP-2), and nitric oxide (NO) or inducible nitric oxide synthase (iNOS), and nuclear factor-kappa B (NF-κB) p65 content in GalN/LPS-treated ICR mice. RAW264 mouse macrophages were used to confirm the anti-inflammatory effects of WTQR and GD on the macrophages.
WTQR and GD increased the survival rate, suppressed the serum aminotransferase activities, serum levels and hepatic gene expression of TNF-α, MIP-2, and NO or iNOS, and nuclear NF-κB p65 content in GalN/LPS-treated mice; decreased the oxidized glutathione content, increased the superoxide dismutase activity, and decreased the histopathological grade values of the hepatocyte necrosis and lobular inflammation in GalN/LPS-injured liver; and suppressed the release levels and gene expression of TNF-α, MIP-2, and NO or iNOS, and nuclear NF-κB p65 content in LPS-stimulated RAW264 macrophages. WTQR and GD may improve the antioxidant defense system and inflammatory status in GalN/LPS-injured liver.
These findings indicate that WTQR and GD have hepatoprotective effects on GalN/LPS-induced liver injury in ICR mice.</description><subject>active ingredients</subject><subject>Analysis of Variance</subject><subject>Animals</subject><subject>anti-inflammatory activity</subject><subject>antioxidants</subject><subject>Antioxidants - metabolism</subject><subject>blood serum</subject><subject>Cell Line</subject><subject>Chemical and Drug Induced Liver Injury - drug therapy</subject><subject>Chemical and Drug Induced Liver Injury - immunology</subject><subject>Chemical and Drug Induced Liver Injury - metabolism</subject><subject>chemokine CXCL2</subject><subject>Chemokine CXCL2 - blood</subject><subject>Chemokine CXCL2 - genetics</subject><subject>enzyme activity</subject><subject>Galactosamine</subject><subject>Galactosamine - administration & dosage</subject><subject>Galactosamine - adverse effects</subject><subject>gene expression</subject><subject>Globin digest</subject><subject>Globins - administration & dosage</subject><subject>Globins - chemistry</subject><subject>glutathione</subject><subject>Hepatocytes - drug effects</subject><subject>Hepatocytes - metabolism</subject><subject>hepatoprotective effect</subject><subject>histopathology</subject><subject>inducible nitric oxide synthase</subject><subject>inflammation</subject><subject>Lipopolysaccharide</subject><subject>lipopolysaccharides</subject><subject>Lipopolysaccharides - administration & dosage</subject><subject>Lipopolysaccharides - adverse effects</subject><subject>liver</subject><subject>Liver - drug effects</subject><subject>Liver - metabolism</subject><subject>Liver - pathology</subject><subject>Liver injury</subject><subject>macrophages</subject><subject>Macrophages - metabolism</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred ICR</subject><subject>necrosis</subject><subject>NF-kappa B - analysis</subject><subject>NF-kappa B - metabolism</subject><subject>nitric oxide</subject><subject>Nitric Oxide - blood</subject><subject>Nitric Oxide - metabolism</subject><subject>Nitric Oxide Synthase Type II - genetics</subject><subject>Nitric Oxide Synthase Type II - metabolism</subject><subject>Oligopeptides - administration & dosage</subject><subject>Peptide Fragments - administration & dosage</subject><subject>Peptide Fragments - chemistry</subject><subject>RAW264</subject><subject>superoxide dismutase</subject><subject>Survival Rate</subject><subject>Transaminases - blood</subject><subject>transcription factor NF-kappa B</subject><subject>Trp-Thr-Gln-Arg (WTQR)</subject><subject>tumor necrosis factor-alpha</subject><subject>Tumor Necrosis Factor-alpha - blood</subject><subject>Tumor Necrosis Factor-alpha - genetics</subject><issn>0024-3205</issn><issn>1879-0631</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kcFq3DAQhkVpaLabPkAvrW49aSPZK9uip7CkSSBQSDZnoZXGjhbZciU7sE-Q1-4sm-ZYGGlA-v8fzSdCvgq-ElxUl_tVaPOq4EKssLgoP5CFaGrFeFWKj2TBebFmZcHlOfmc855zLmVdfiLnRSHkWvFqQV6v2xbslGlsaRfizg_U-Q7yRM3gqMcLYyf_AtQPXQLnYZjoNo1s-5zYTRjYVepoHGhnAupiNr0f4DL4MY4xHLKx9tkk74D5wc0WHA2YlTBsP6cDNnq3eaC9t3BBzloTMnx560vy9Ot6u7ll979v7jZX98wWSkxsXTdyVymlaiFq62xlbA0OQOKQvJA4lpKOC6uUa6RclxWqVIN7AzuHx-WS_Djljin-mXFO3ftsIQQzQJyzVqKWdVUiyyURJ6VNMecErR6T7006aMH1Eb_ea8Svj_g1FlrQ8-0tfd714N4d_3ij4PtJ0JqoTZd81k-PmCA5LqGaY8TPkwKQwouHpLNF6sjOJ_wo7aL_zwP-At3QnyA</recordid><startdate>20120130</startdate><enddate>20120130</enddate><creator>Sasakawa, Yuka</creator><creator>Kominami, Akari</creator><creator>Yamamoto, Kaori</creator><creator>Nakaoka, Fumiko</creator><creator>Nakamura, Miki</creator><creator>Nakao, Mayumi</creator><creator>Abe, Michiyo</creator><creator>Fukuhama, Chizuko</creator><creator>Kagawa, Kyoichi</creator><general>Elsevier Inc</general><scope>FBQ</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>20120130</creationdate><title>Effects of globin digest and its active ingredient Trp-Thr-Gln-Arg on galactosamine/lipopolysaccharide-induced liver injury in ICR mice</title><author>Sasakawa, Yuka ; Kominami, Akari ; Yamamoto, Kaori ; Nakaoka, Fumiko ; Nakamura, Miki ; Nakao, Mayumi ; Abe, Michiyo ; Fukuhama, Chizuko ; Kagawa, Kyoichi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c291t-4785b69997117cdc6ac7edee520502521595d01c99d85543617c986178ebd1c93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>active ingredients</topic><topic>Analysis of Variance</topic><topic>Animals</topic><topic>anti-inflammatory activity</topic><topic>antioxidants</topic><topic>Antioxidants - metabolism</topic><topic>blood serum</topic><topic>Cell Line</topic><topic>Chemical and Drug Induced Liver Injury - drug therapy</topic><topic>Chemical and Drug Induced Liver Injury - immunology</topic><topic>Chemical and Drug Induced Liver Injury - metabolism</topic><topic>chemokine CXCL2</topic><topic>Chemokine CXCL2 - blood</topic><topic>Chemokine CXCL2 - genetics</topic><topic>enzyme activity</topic><topic>Galactosamine</topic><topic>Galactosamine - administration & dosage</topic><topic>Galactosamine - adverse effects</topic><topic>gene expression</topic><topic>Globin digest</topic><topic>Globins - administration & dosage</topic><topic>Globins - chemistry</topic><topic>glutathione</topic><topic>Hepatocytes - drug effects</topic><topic>Hepatocytes - metabolism</topic><topic>hepatoprotective effect</topic><topic>histopathology</topic><topic>inducible nitric oxide synthase</topic><topic>inflammation</topic><topic>Lipopolysaccharide</topic><topic>lipopolysaccharides</topic><topic>Lipopolysaccharides - administration & dosage</topic><topic>Lipopolysaccharides - adverse effects</topic><topic>liver</topic><topic>Liver - drug effects</topic><topic>Liver - metabolism</topic><topic>Liver - pathology</topic><topic>Liver injury</topic><topic>macrophages</topic><topic>Macrophages - metabolism</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred ICR</topic><topic>necrosis</topic><topic>NF-kappa B - analysis</topic><topic>NF-kappa B - metabolism</topic><topic>nitric oxide</topic><topic>Nitric Oxide - blood</topic><topic>Nitric Oxide - metabolism</topic><topic>Nitric Oxide Synthase Type II - genetics</topic><topic>Nitric Oxide Synthase Type II - metabolism</topic><topic>Oligopeptides - administration & dosage</topic><topic>Peptide Fragments - administration & dosage</topic><topic>Peptide Fragments - chemistry</topic><topic>RAW264</topic><topic>superoxide dismutase</topic><topic>Survival Rate</topic><topic>Transaminases - blood</topic><topic>transcription factor NF-kappa B</topic><topic>Trp-Thr-Gln-Arg (WTQR)</topic><topic>tumor necrosis factor-alpha</topic><topic>Tumor Necrosis Factor-alpha - blood</topic><topic>Tumor Necrosis Factor-alpha - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sasakawa, Yuka</creatorcontrib><creatorcontrib>Kominami, Akari</creatorcontrib><creatorcontrib>Yamamoto, Kaori</creatorcontrib><creatorcontrib>Nakaoka, Fumiko</creatorcontrib><creatorcontrib>Nakamura, Miki</creatorcontrib><creatorcontrib>Nakao, Mayumi</creatorcontrib><creatorcontrib>Abe, Michiyo</creatorcontrib><creatorcontrib>Fukuhama, Chizuko</creatorcontrib><creatorcontrib>Kagawa, Kyoichi</creatorcontrib><collection>AGRIS</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>Life sciences (1973)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sasakawa, Yuka</au><au>Kominami, Akari</au><au>Yamamoto, Kaori</au><au>Nakaoka, Fumiko</au><au>Nakamura, Miki</au><au>Nakao, Mayumi</au><au>Abe, Michiyo</au><au>Fukuhama, Chizuko</au><au>Kagawa, Kyoichi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effects of globin digest and its active ingredient Trp-Thr-Gln-Arg on galactosamine/lipopolysaccharide-induced liver injury in ICR mice</atitle><jtitle>Life sciences (1973)</jtitle><addtitle>Life Sci</addtitle><date>2012-01-30</date><risdate>2012</risdate><volume>90</volume><issue>5-6</issue><spage>190</spage><epage>199</epage><pages>190-199</pages><issn>0024-3205</issn><eissn>1879-0631</eissn><abstract>We investigated the effects of globin digest (GD) and its active ingredient Trp-Thr-Gln-Arg (WTQR) on galactosamine/lipopolysaccharide (GalN/LPS)-induced liver injury in imprinting control region (ICR) mice.
The effects of WTQR and GD on the liver injury were examined by measuring the survival rate, serum aminotransferase activities, hepatic components, antioxidant enzyme activities, histopathological analysis, serum levels and hepatic gene expression of tumor necrosis factor-alpha (TNF-α), macrophage inflammatory protein-2 (MIP-2), and nitric oxide (NO) or inducible nitric oxide synthase (iNOS), and nuclear factor-kappa B (NF-κB) p65 content in GalN/LPS-treated ICR mice. RAW264 mouse macrophages were used to confirm the anti-inflammatory effects of WTQR and GD on the macrophages.
WTQR and GD increased the survival rate, suppressed the serum aminotransferase activities, serum levels and hepatic gene expression of TNF-α, MIP-2, and NO or iNOS, and nuclear NF-κB p65 content in GalN/LPS-treated mice; decreased the oxidized glutathione content, increased the superoxide dismutase activity, and decreased the histopathological grade values of the hepatocyte necrosis and lobular inflammation in GalN/LPS-injured liver; and suppressed the release levels and gene expression of TNF-α, MIP-2, and NO or iNOS, and nuclear NF-κB p65 content in LPS-stimulated RAW264 macrophages. WTQR and GD may improve the antioxidant defense system and inflammatory status in GalN/LPS-injured liver.
These findings indicate that WTQR and GD have hepatoprotective effects on GalN/LPS-induced liver injury in ICR mice.</abstract><cop>Netherlands</cop><pub>Elsevier Inc</pub><pmid>22154906</pmid><doi>10.1016/j.lfs.2011.11.013</doi><tpages>10</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0024-3205 |
| ispartof | Life sciences (1973), 2012-01, Vol.90 (5-6), p.190-199 |
| issn | 0024-3205 1879-0631 |
| language | eng |
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| subjects | active ingredients Analysis of Variance Animals anti-inflammatory activity antioxidants Antioxidants - metabolism blood serum Cell Line Chemical and Drug Induced Liver Injury - drug therapy Chemical and Drug Induced Liver Injury - immunology Chemical and Drug Induced Liver Injury - metabolism chemokine CXCL2 Chemokine CXCL2 - blood Chemokine CXCL2 - genetics enzyme activity Galactosamine Galactosamine - administration & dosage Galactosamine - adverse effects gene expression Globin digest Globins - administration & dosage Globins - chemistry glutathione Hepatocytes - drug effects Hepatocytes - metabolism hepatoprotective effect histopathology inducible nitric oxide synthase inflammation Lipopolysaccharide lipopolysaccharides Lipopolysaccharides - administration & dosage Lipopolysaccharides - adverse effects liver Liver - drug effects Liver - metabolism Liver - pathology Liver injury macrophages Macrophages - metabolism Male Mice Mice, Inbred ICR necrosis NF-kappa B - analysis NF-kappa B - metabolism nitric oxide Nitric Oxide - blood Nitric Oxide - metabolism Nitric Oxide Synthase Type II - genetics Nitric Oxide Synthase Type II - metabolism Oligopeptides - administration & dosage Peptide Fragments - administration & dosage Peptide Fragments - chemistry RAW264 superoxide dismutase Survival Rate Transaminases - blood transcription factor NF-kappa B Trp-Thr-Gln-Arg (WTQR) tumor necrosis factor-alpha Tumor Necrosis Factor-alpha - blood Tumor Necrosis Factor-alpha - genetics |
| title | Effects of globin digest and its active ingredient Trp-Thr-Gln-Arg on galactosamine/lipopolysaccharide-induced liver injury in ICR mice |
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