{"@context":{"@vocab":"https://cir.nii.ac.jp/schema/1.0/","rdfs":"http://www.w3.org/2000/01/rdf-schema#","dc":"http://purl.org/dc/elements/1.1/","dcterms":"http://purl.org/dc/terms/","foaf":"http://xmlns.com/foaf/0.1/","prism":"http://prismstandard.org/namespaces/basic/2.0/","cinii":"http://ci.nii.ac.jp/ns/1.0/","datacite":"https://schema.datacite.org/meta/kernel-4/","ndl":"http://ndl.go.jp/dcndl/terms/","jpcoar":"https://github.com/JPCOAR/schema/blob/master/2.0/"},"@id":"https://cir.nii.ac.jp/crid/1390282679879124992.json","@type":"Article","productIdentifier":[{"identifier":{"@type":"DOI","@value":"10.2131/jts.30.157"}},{"identifier":{"@type":"PMID","@value":"16141650"}},{"identifier":{"@type":"NDL_BIB_ID","@value":"7474062"}},{"identifier":{"@type":"URI","@value":"http://id.ndl.go.jp/bib/7474062"}},{"identifier":{"@type":"URI","@value":"https://ndlsearch.ndl.go.jp/books/R000000004-I7474062"}},{"identifier":{"@type":"URI","@value":"http://www.jstage.jst.go.jp/article/jts/30/3/30_3_157/_pdf"}},{"identifier":{"@type":"NAID","@value":"110001828228"}},{"identifier":{"@type":"URI","@value":"https://search.jamas.or.jp/link/ui/2006293581"}}],"resourceType":"学術雑誌論文(journal article)","dc:title":[{"@language":"en","@value":"PROTECTIVE EFFECT OF A PROTEIN KINASE INHIBITOR ON CELLULAR INJURY INDUCED BY CEPHALORIDINE IN THE PORCINE KIDNEY CELL LINE LLC-PK1"}],"dc:language":"en","description":[{"type":"abstract","notation":[{"@language":"en","@value":"We investigated the effects of a protein kinase C inhibitor and a tyrosine kinase inhibitor on the cellular injury induced by cephaloridine in an established renal epithelial cell line, LLC-PK<sub>1</sub>. Cephaloridine increased the leakage of lactate dehydrogenase (LDH) from LLC-PK<sub>1</sub> cells into the medium and also caused an increase in the level of lipid peroxide (index of oxidative stress) in the cells. Treatment of the cells with a hydroxyl radical scavenger, dimethylthiourea (DMTU), inhibited the increases in LDH leakage and lipid peroxidation in LLC-PK<sub>1</sub> cells exposed to cephaloridine. A protein kinase C inhibitor, H-7, and tyrosine kinase inhibitors, genistein and lavendustinA, inhibited the increases in LDH leakage and lipid peroxidation in LLC-PK<sub>1</sub> cells exposed to cephaloridine. These results suggest that a signaling pathway which involves protein kinase C and tyrosine kinase plays a role in the generation of reactive oxygen species in LLC-PK<sub>1</sub> cells damaged by cephaloridine.<br>"}],"abstractLicenseFlag":"disallow"}],"creator":[{"@id":"https://cir.nii.ac.jp/crid/1410282679879124994","@type":"Researcher","personIdentifier":[{"@type":"NRID","@value":"9000021572223"}],"foaf:name":[{"@language":"en","@value":"KAWAI Yoshiko"}],"jpcoar:affiliationName":[{"@language":"en","@value":"Division of Pharmacology, Osaka University of Pharmaceutical Science"}]},{"@id":"https://cir.nii.ac.jp/crid/1410282679879124995","@type":"Researcher","personIdentifier":[{"@type":"NRID","@value":"9000021572228"}],"foaf:name":[{"@language":"en","@value":"KOHDA Yuka"}],"jpcoar:affiliationName":[{"@language":"en","@value":"Division of Pharmacology, Osaka University of Pharmaceutical Science"}]},{"@id":"https://cir.nii.ac.jp/crid/1410282679879124992","@type":"Researcher","personIdentifier":[{"@type":"NRID","@value":"9000021572238"}],"foaf:name":[{"@language":"en","@value":"GEMBA Munekazu"}],"jpcoar:affiliationName":[{"@language":"en","@value":"Division of Pharmacology, Osaka University of Pharmaceutical Science"}]},{"@id":"https://cir.nii.ac.jp/crid/1410282679879124993","@type":"Researcher","personIdentifier":[{"@type":"NRID","@value":"9000021572233"}],"foaf:name":[{"@language":"en","@value":"KODAWARA Takaaki"}],"jpcoar:affiliationName":[{"@language":"en","@value":"Division of Pharmacology, Osaka University of Pharmaceutical Science"}]}],"publication":{"publicationIdentifier":[{"@type":"PISSN","@value":"03881350"},{"@type":"LISSN","@value":"03881350"},{"@type":"EISSN","@value":"18803989"},{"@type":"NDL_BIB_ID","@value":"000000032748"},{"@type":"ISSN","@value":"03881350"},{"@type":"NCID","@value":"AN00002808"}],"prism:publicationName":[{"@language":"en","@value":"The Journal of Toxicological Sciences"},{"@language":"ja","@value":"Ｔｈｅ　Ｊｏｕｒｎａｌ　ｏｆ　Ｔｏｘｉｃｏｌｏｇｉｃａｌ　Ｓｃｉｅｎｃｅｓ"},{"@language":"en","@value":"J. Toxicol. Sci."}],"dc:publisher":[{"@language":"en","@value":"The Japanese Society of Toxicology"},{"@language":"ja","@value":"一般社団法人　日本毒性学会"}],"prism:publicationDate":"2005","prism:volume":"30","prism:number":"3","prism:startingPage":"157","prism:endingPage":"163"},"reviewed":"false","dcterms:accessRights":"http://purl.org/coar/access_right/c_abf2","url":[{"@id":"http://id.ndl.go.jp/bib/7474062"},{"@id":"https://ndlsearch.ndl.go.jp/books/R000000004-I7474062"},{"@id":"http://www.jstage.jst.go.jp/article/jts/30/3/30_3_157/_pdf"},{"@id":"https://search.jamas.or.jp/link/ui/2006293581"}],"availableAt":"2005","foaf:topic":[{"@id":"https://cir.nii.ac.jp/all?q=Nephrotoxicity","dc:title":"Nephrotoxicity"},{"@id":"https://cir.nii.ac.jp/all?q=Renal%20epithelial%20cells","dc:title":"Renal epithelial cells"},{"@id":"https://cir.nii.ac.jp/all?q=Cephaloridine","dc:title":"Cephaloridine"},{"@id":"https://cir.nii.ac.jp/all?q=Protein%20kinase%20C","dc:title":"Protein kinase C"},{"@id":"https://cir.nii.ac.jp/all?q=Tyrosine%20kinase","dc:title":"Tyrosine kinase"},{"@id":"https://cir.nii.ac.jp/all?q=Oxidative%20stress","dc:title":"Oxidative stress"}],"relatedProduct":[{"@id":"https://cir.nii.ac.jp/crid/1360011145392007424","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Relationship between the Transport and Toxicity of Cephalosporins in the Kidney"}]},{"@id":"https://cir.nii.ac.jp/crid/1360292618581936768","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Cytochrome b\n            <sub>558</sub>\n            : the Flavin-Binding Component of the Phagocyte NADPH Oxidase"}]},{"@id":"https://cir.nii.ac.jp/crid/1360292618663054080","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Role of redox potential and reactive oxygen species in stress 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