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Curcumin ameliorates cisplatin-induced nephrotoxicity by inhibiting renal inflammation in mice
Inflammatory mechanisms may play an important role in the pathogenesis of cisplatin-induced nephrotoxicity. Curcumin is an orange-yellow polyphenol present in curry spice and has anti-inflammatory and antioxidant effects. The purpose of this study was to determine the protective effects of curcumin...
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Published in: | Journal of bioscience and bioengineering 2013-05, Vol.115 (5), p.547-551 |
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description | Inflammatory mechanisms may play an important role in the pathogenesis of cisplatin-induced nephrotoxicity. Curcumin is an orange-yellow polyphenol present in curry spice and has anti-inflammatory and antioxidant effects. The purpose of this study was to determine the protective effects of curcumin on cisplatin-induced nephrotoxicity. Mice were randomly divided into four groups: control, cisplatin, cisplatin + curcumin and curcumin. Mice were given cisplatin (20 mg/kg body weight, intraperitoneally) with or without curcumin treatment (100 mg/kg body weight, intraperitoneally, immediately after cisplatin injection). Serum and renal tumor necrosis factor (TNF)-alpha and renal monocyte chemoattractant protein (MCP)-1 concentrations, intercellular adhesion molecule-1 (ICAM-1) mRNA expression in kidney, renal function and histological changes were determined 72 h after cisplatin injection. Serum TNF-alpha concentration in the cisplatin + curcumin group significantly decreased compared with that in the cisplatin group. Renal TNF-alpha and MCP-1 concentrations and ICAM-1 mRNA expression in kidney in the cisplatin + curcumin group also significantly decreased compared with those in the cisplatin group. Consequently, cisplatin-induced renal dysfunction and renal tubular necrosis scores were attenuated by curcumin treatment. These results indicate that curcumin acts to reduce cisplatin-induced nephrotoxicity through its anti-inflammatory effects. Thus, curcumin may become a new therapeutic candidate for the treatment of cisplatin-induced nephrotoxicity. |
doi_str_mv | 10.1016/j.jbiosc.2012.11.007 |
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Curcumin is an orange-yellow polyphenol present in curry spice and has anti-inflammatory and antioxidant effects. The purpose of this study was to determine the protective effects of curcumin on cisplatin-induced nephrotoxicity. Mice were randomly divided into four groups: control, cisplatin, cisplatin + curcumin and curcumin. Mice were given cisplatin (20 mg/kg body weight, intraperitoneally) with or without curcumin treatment (100 mg/kg body weight, intraperitoneally, immediately after cisplatin injection). Serum and renal tumor necrosis factor (TNF)-alpha and renal monocyte chemoattractant protein (MCP)-1 concentrations, intercellular adhesion molecule-1 (ICAM-1) mRNA expression in kidney, renal function and histological changes were determined 72 h after cisplatin injection. Serum TNF-alpha concentration in the cisplatin + curcumin group significantly decreased compared with that in the cisplatin group. Renal TNF-alpha and MCP-1 concentrations and ICAM-1 mRNA expression in kidney in the cisplatin + curcumin group also significantly decreased compared with those in the cisplatin group. Consequently, cisplatin-induced renal dysfunction and renal tubular necrosis scores were attenuated by curcumin treatment. These results indicate that curcumin acts to reduce cisplatin-induced nephrotoxicity through its anti-inflammatory effects. Thus, curcumin may become a new therapeutic candidate for the treatment of cisplatin-induced nephrotoxicity.</description><identifier>ISSN: 1389-1723</identifier><identifier>EISSN: 1347-4421</identifier><identifier>DOI: 10.1016/j.jbiosc.2012.11.007</identifier><identifier>PMID: 23245727</identifier><language>eng</language><publisher>Amsterdam: Elsevier B.V</publisher><subject>Acute Kidney Injury - chemically induced ; Acute Kidney Injury - metabolism ; Acute Kidney Injury - prevention & control ; adhesion ; Animals ; anti-inflammatory activity ; Anti-Inflammatory Agents - pharmacology ; Anti-Inflammatory Agents - therapeutic use ; Antineoplastic Agents - toxicity ; antioxidant activity ; Antioxidants ; Antioxidants - pharmacology ; Antioxidants - therapeutic use ; Biological and medical sciences ; Biotechnology ; blood serum ; body weight ; chemoattractants ; Chemokine CCL2 - metabolism ; Chemokines ; Cisplatin ; Cisplatin - toxicity ; Curcumin ; Curcumin - pharmacology ; Curcumin - therapeutic use ; curry ; Fundamental and applied biological sciences. Psychology ; gene expression ; inflammation ; Inflammation - drug therapy ; Intercellular Adhesion Molecule-1 - genetics ; Intercellular Adhesion Molecule-1 - metabolism ; Kidney - drug effects ; Kidney - metabolism ; Kidney - pathology ; kidneys ; Male ; messenger RNA ; Mice ; Mice, Inbred C57BL ; monocytes ; necrosis ; Nephrotoxicity ; pathogenesis ; polyphenols ; protective effect ; renal function ; Tumor necrosis factor alpha ; Tumor Necrosis Factor-alpha - blood ; Tumor Necrosis Factor-alpha - metabolism</subject><ispartof>Journal of bioscience and bioengineering, 2013-05, Vol.115 (5), p.547-551</ispartof><rights>2012 The Society for Biotechnology, Japan</rights><rights>2014 INIST-CNRS</rights><rights>Copyright © 2012 The Society for Biotechnology, Japan. Published by Elsevier B.V. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c566t-361ddae1814e77469826ad6a666282c03d2c80be3459c982a9ec2349e2f1c16e3</citedby><cites>FETCH-LOGICAL-c566t-361ddae1814e77469826ad6a666282c03d2c80be3459c982a9ec2349e2f1c16e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27903,27904</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=27411419$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23245727$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ueki, Masaaki</creatorcontrib><creatorcontrib>Ueno, Masaki</creatorcontrib><creatorcontrib>Morishita, Jun</creatorcontrib><creatorcontrib>Maekawa, Nobuhiro</creatorcontrib><title>Curcumin ameliorates cisplatin-induced nephrotoxicity by inhibiting renal inflammation in mice</title><title>Journal of bioscience and bioengineering</title><addtitle>J Biosci Bioeng</addtitle><description>Inflammatory mechanisms may play an important role in the pathogenesis of cisplatin-induced nephrotoxicity. Curcumin is an orange-yellow polyphenol present in curry spice and has anti-inflammatory and antioxidant effects. The purpose of this study was to determine the protective effects of curcumin on cisplatin-induced nephrotoxicity. Mice were randomly divided into four groups: control, cisplatin, cisplatin + curcumin and curcumin. Mice were given cisplatin (20 mg/kg body weight, intraperitoneally) with or without curcumin treatment (100 mg/kg body weight, intraperitoneally, immediately after cisplatin injection). Serum and renal tumor necrosis factor (TNF)-alpha and renal monocyte chemoattractant protein (MCP)-1 concentrations, intercellular adhesion molecule-1 (ICAM-1) mRNA expression in kidney, renal function and histological changes were determined 72 h after cisplatin injection. Serum TNF-alpha concentration in the cisplatin + curcumin group significantly decreased compared with that in the cisplatin group. Renal TNF-alpha and MCP-1 concentrations and ICAM-1 mRNA expression in kidney in the cisplatin + curcumin group also significantly decreased compared with those in the cisplatin group. Consequently, cisplatin-induced renal dysfunction and renal tubular necrosis scores were attenuated by curcumin treatment. These results indicate that curcumin acts to reduce cisplatin-induced nephrotoxicity through its anti-inflammatory effects. Thus, curcumin may become a new therapeutic candidate for the treatment of cisplatin-induced nephrotoxicity.</description><subject>Acute Kidney Injury - chemically induced</subject><subject>Acute Kidney Injury - metabolism</subject><subject>Acute Kidney Injury - prevention & control</subject><subject>adhesion</subject><subject>Animals</subject><subject>anti-inflammatory activity</subject><subject>Anti-Inflammatory Agents - pharmacology</subject><subject>Anti-Inflammatory Agents - therapeutic use</subject><subject>Antineoplastic Agents - toxicity</subject><subject>antioxidant activity</subject><subject>Antioxidants</subject><subject>Antioxidants - pharmacology</subject><subject>Antioxidants - therapeutic use</subject><subject>Biological and medical sciences</subject><subject>Biotechnology</subject><subject>blood serum</subject><subject>body weight</subject><subject>chemoattractants</subject><subject>Chemokine CCL2 - metabolism</subject><subject>Chemokines</subject><subject>Cisplatin</subject><subject>Cisplatin - toxicity</subject><subject>Curcumin</subject><subject>Curcumin - pharmacology</subject><subject>Curcumin - therapeutic use</subject><subject>curry</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>gene expression</subject><subject>inflammation</subject><subject>Inflammation - drug therapy</subject><subject>Intercellular Adhesion Molecule-1 - genetics</subject><subject>Intercellular Adhesion Molecule-1 - metabolism</subject><subject>Kidney - drug effects</subject><subject>Kidney - metabolism</subject><subject>Kidney - pathology</subject><subject>kidneys</subject><subject>Male</subject><subject>messenger RNA</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>monocytes</subject><subject>necrosis</subject><subject>Nephrotoxicity</subject><subject>pathogenesis</subject><subject>polyphenols</subject><subject>protective effect</subject><subject>renal function</subject><subject>Tumor necrosis factor alpha</subject><subject>Tumor Necrosis Factor-alpha - blood</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><issn>1389-1723</issn><issn>1347-4421</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><recordid>eNp9kU2P1SAUhonROB_6D4x2Y-KmlQMUysbE3OhoMokLna2E0tMZblq4Qmu8_15uetWdK76e9xzyHEJeAG2Agny7b_a9j9k1jAJrABpK1SNyCVyoWggGj0_7TtegGL8gVznvKQVFFTwlF4wz0SqmLsn33ZrcOvtQ2RknH5NdMFfO58NkFx9qH4bV4VAFPDykuMRf3vnlWPXHyocH3_vC3FcJg53KxTjZeS6xGMqhmr3DZ-TJaKeMz8_rNbn7-OHb7lN9--Xm8-79be1aKZeaSxgGi9CBQKWE1B2TdpBWSsk65igfmOtoj1y02pVHq9ExLjSyERxI5NfkzVb3kOKPFfNiZp8dTpMNGNdsgLeMaaaFKKjYUJdizglHc0h-tulogJqTWbM3m1lzMmsATDFbYi_PHdZ-xuFv6I_KArw-AzY7O43JhqLxH6cEgABduFcbN9po7H0qzN3X0knSMh_NWFuIdxuBxdhPj8lk5zGUMfiEbjFD9P__62-P86Ks</recordid><startdate>20130501</startdate><enddate>20130501</enddate><creator>Ueki, Masaaki</creator><creator>Ueno, Masaki</creator><creator>Morishita, Jun</creator><creator>Maekawa, Nobuhiro</creator><general>Elsevier B.V</general><general>Elsevier</general><scope>FBQ</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>7QO</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>P64</scope></search><sort><creationdate>20130501</creationdate><title>Curcumin ameliorates cisplatin-induced nephrotoxicity by inhibiting renal inflammation in mice</title><author>Ueki, Masaaki ; Ueno, Masaki ; Morishita, Jun ; Maekawa, Nobuhiro</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c566t-361ddae1814e77469826ad6a666282c03d2c80be3459c982a9ec2349e2f1c16e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Acute Kidney Injury - chemically induced</topic><topic>Acute Kidney Injury - metabolism</topic><topic>Acute Kidney Injury - prevention & control</topic><topic>adhesion</topic><topic>Animals</topic><topic>anti-inflammatory activity</topic><topic>Anti-Inflammatory Agents - pharmacology</topic><topic>Anti-Inflammatory Agents - therapeutic use</topic><topic>Antineoplastic Agents - toxicity</topic><topic>antioxidant activity</topic><topic>Antioxidants</topic><topic>Antioxidants - pharmacology</topic><topic>Antioxidants - therapeutic use</topic><topic>Biological and medical sciences</topic><topic>Biotechnology</topic><topic>blood serum</topic><topic>body weight</topic><topic>chemoattractants</topic><topic>Chemokine CCL2 - metabolism</topic><topic>Chemokines</topic><topic>Cisplatin</topic><topic>Cisplatin - toxicity</topic><topic>Curcumin</topic><topic>Curcumin - pharmacology</topic><topic>Curcumin - therapeutic use</topic><topic>curry</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>gene expression</topic><topic>inflammation</topic><topic>Inflammation - drug therapy</topic><topic>Intercellular Adhesion Molecule-1 - genetics</topic><topic>Intercellular Adhesion Molecule-1 - metabolism</topic><topic>Kidney - drug effects</topic><topic>Kidney - metabolism</topic><topic>Kidney - pathology</topic><topic>kidneys</topic><topic>Male</topic><topic>messenger RNA</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>monocytes</topic><topic>necrosis</topic><topic>Nephrotoxicity</topic><topic>pathogenesis</topic><topic>polyphenols</topic><topic>protective effect</topic><topic>renal function</topic><topic>Tumor necrosis factor alpha</topic><topic>Tumor Necrosis Factor-alpha - blood</topic><topic>Tumor Necrosis Factor-alpha - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ueki, Masaaki</creatorcontrib><creatorcontrib>Ueno, Masaki</creatorcontrib><creatorcontrib>Morishita, Jun</creatorcontrib><creatorcontrib>Maekawa, Nobuhiro</creatorcontrib><collection>AGRIS</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>Biotechnology Research Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><jtitle>Journal of bioscience and bioengineering</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ueki, Masaaki</au><au>Ueno, Masaki</au><au>Morishita, Jun</au><au>Maekawa, Nobuhiro</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Curcumin ameliorates cisplatin-induced nephrotoxicity by inhibiting renal inflammation in mice</atitle><jtitle>Journal of bioscience and bioengineering</jtitle><addtitle>J Biosci Bioeng</addtitle><date>2013-05-01</date><risdate>2013</risdate><volume>115</volume><issue>5</issue><spage>547</spage><epage>551</epage><pages>547-551</pages><issn>1389-1723</issn><eissn>1347-4421</eissn><abstract>Inflammatory mechanisms may play an important role in the pathogenesis of cisplatin-induced nephrotoxicity. Curcumin is an orange-yellow polyphenol present in curry spice and has anti-inflammatory and antioxidant effects. The purpose of this study was to determine the protective effects of curcumin on cisplatin-induced nephrotoxicity. Mice were randomly divided into four groups: control, cisplatin, cisplatin + curcumin and curcumin. Mice were given cisplatin (20 mg/kg body weight, intraperitoneally) with or without curcumin treatment (100 mg/kg body weight, intraperitoneally, immediately after cisplatin injection). Serum and renal tumor necrosis factor (TNF)-alpha and renal monocyte chemoattractant protein (MCP)-1 concentrations, intercellular adhesion molecule-1 (ICAM-1) mRNA expression in kidney, renal function and histological changes were determined 72 h after cisplatin injection. Serum TNF-alpha concentration in the cisplatin + curcumin group significantly decreased compared with that in the cisplatin group. Renal TNF-alpha and MCP-1 concentrations and ICAM-1 mRNA expression in kidney in the cisplatin + curcumin group also significantly decreased compared with those in the cisplatin group. Consequently, cisplatin-induced renal dysfunction and renal tubular necrosis scores were attenuated by curcumin treatment. These results indicate that curcumin acts to reduce cisplatin-induced nephrotoxicity through its anti-inflammatory effects. Thus, curcumin may become a new therapeutic candidate for the treatment of cisplatin-induced nephrotoxicity.</abstract><cop>Amsterdam</cop><pub>Elsevier B.V</pub><pmid>23245727</pmid><doi>10.1016/j.jbiosc.2012.11.007</doi><tpages>5</tpages></addata></record> |
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subjects | Acute Kidney Injury - chemically induced Acute Kidney Injury - metabolism Acute Kidney Injury - prevention & control adhesion Animals anti-inflammatory activity Anti-Inflammatory Agents - pharmacology Anti-Inflammatory Agents - therapeutic use Antineoplastic Agents - toxicity antioxidant activity Antioxidants Antioxidants - pharmacology Antioxidants - therapeutic use Biological and medical sciences Biotechnology blood serum body weight chemoattractants Chemokine CCL2 - metabolism Chemokines Cisplatin Cisplatin - toxicity Curcumin Curcumin - pharmacology Curcumin - therapeutic use curry Fundamental and applied biological sciences. Psychology gene expression inflammation Inflammation - drug therapy Intercellular Adhesion Molecule-1 - genetics Intercellular Adhesion Molecule-1 - metabolism Kidney - drug effects Kidney - metabolism Kidney - pathology kidneys Male messenger RNA Mice Mice, Inbred C57BL monocytes necrosis Nephrotoxicity pathogenesis polyphenols protective effect renal function Tumor necrosis factor alpha Tumor Necrosis Factor-alpha - blood Tumor Necrosis Factor-alpha - metabolism |
title | Curcumin ameliorates cisplatin-induced nephrotoxicity by inhibiting renal inflammation in mice |
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