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dc.contributor.authorHabibi, RM
dc.contributor.authorGhasemipour, Z
dc.contributor.authorHalabian, R
dc.contributor.authorMohammadi, RA
dc.contributor.authorYaghmai, P
dc.contributor.authorGharehbaghian, A
dc.contributor.authorOodi, A
dc.contributor.authorMassrori, N
dc.contributor.authorAmirizadeh, N
dc.contributor.authorShokrgozar, MA
dc.date.accessioned2018-08-26T08:27:54Z
dc.date.available2018-08-26T08:27:54Z
dc.date.issued2008
dc.identifier.urihttp://dspace.tbzmed.ac.ir:8080/xmlui/handle/123456789/51315
dc.description.abstractBackground and the purpose of the study: Lipocalin 2 (Lcn2, NGAL) is a member of the lipocalin super family which has been known as an early marker for ischemic acute renal injury and cisplatin nephrortoxicity. In this study the ability of Lcn2 to prevent cisplatin-induced toxicity was studied. Methods: Lcn2 cDNA was isolated from Hep G2 cell line and cloned to pcDNA3.1(+) vector. The construct was trasnfected to CHO cell line. Stable clones were generated and the expression of Lcn2 was determined by RT-PCR and ELISA. Lcn2 gene in A549 cell line was also down-regulated with the siRNA. CHO and A549 cells were exposed to cisplatin and cell proliferation was determined by MTT assay. Results: Cell proliferation was higher in CHO expressing Lcn2 at doses of 75, 150, and 200 mu g/ml of cisplatin after 48 h compared with control. Cisplatin toxicity increased significantly in A549 cells following treatment with Lcn2 siRNA. Major conclusion: findings of this study revealed that Lcn2 acts as a cytoprotective factor against cisplatin toxicity and suggests that Lcn2 might have the potential application to ameliorate the cisplatin toxicity.
dc.language.isoEnglish
dc.relation.ispartofDARU-JOURNAL OF PHARMACEUTICAL SCIENCES
dc.subjectLcn2/NGAL
dc.subjectcisplatin
dc.subjecttoxicity
dc.subjectcytoprotective factor
dc.titleLipocalin 2 acts as a cytoprotective factor against cisplatin toxicity, an in vitro study
dc.typeArticle
dc.citation.volume16
dc.citation.issue2
dc.citation.spage106
dc.citation.epage111
dc.citation.indexWeb of science


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