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Vol. 31, No. 2, 2010
Issue release date: February 2010
Section title: Original Report: Laboratory Investigation
Am J Nephrol 2010;31:178–188
(DOI:10.1159/000268161)

N-Acetylcysteine Amide Protects Renal Proximal Tubular Epithelial Cells against Iohexol-Induced Apoptosis by Blocking p38 MAPK and iNOS Signaling

Gong X.a, d · Celsi G.a · Carlsson K.c · Norgren S.c · Chen M.b
Divisions of aPediatric Nephrology and bRadiology C1:46, Department of Clinical Science, Intervention and Technology, and cDivision of Pediatric Endocrinology B57, Department of Woman and Child Health, Karolinska Institutet, Karolinska University Hospital Huddinge, Stockholm, Sweden; dDepartment of Nephrology, Shanghai Hospital of Traditional Chinese Medicine, Shanghai, China

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Article / Publication Details

First-Page Preview
Abstract of Original Report: Laboratory Investigation

Received: 4/14/2009
Accepted: 11/2/2009
Published online: 12/17/2009
Issue release date: February 2010

Number of Print Pages: 11
Number of Figures: 8
Number of Tables: 0

ISSN: 0250-8095 (Print)
eISSN: 1421-9670 (Online)

For additional information: http://www.karger.com/AJN

Abstract

Background: The pathogenesis of contrast-induced nephropathy (CIN) is still poorly understood and apoptosis via oxidative stress has been proposed as one possible mechanism. We therefore studied the apoptotic signaling mechanism in CIN and also tested whether the new antioxidant N-acetylcysteine amide (NACA) could prevent CIN. Methods: LLC-PK1 cells were exposed to a widely used contrast agent, iohexol (IH). Cytotoxicity was assessed with morphology and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Cell death was analyzed by the DNA content analysis and PARP cleavage. Protein expression was assessed with Western blotting. Results: We observed cell death with apoptotic features in a dose- and time-dependent manner. Initiation of IH-induced apoptosis was mediated by upregulation of Bax and downregulation of Bcl-2 and Mcl-1, which was preceded by p38 MAPK activation and iNOS induction. Inhibitors of p38 MAPK and iNOS partially abolished IH-induced apoptosis. Furthermore, we found pretreatment with NACA partially protected cells from IH-induced death by reverting the expression of Bcl-2, Mc1-1 and Bax expression through inhibition of p38 MAPK and iNOS pathway. Conclusions: This study demonstrates that apoptosis occurs during CIN. Apoptosis is associated with activations of p38 MAPK and iNOS. Pretreatment with the antioxidant NACA could prevent IH-induced cell death by blocking the p38 MAPK/iNOS signaling pathway.

© 2009 S. Karger AG, Basel


  

Author Contacts

Xuezhong Gong
Department of Nephrology, Shanghai Hospital of Traditional Chinese Medicine
274 Zhijiang Middle Road, Shanghai 20071 (China)
Tel. +86 21 5663 9828, ext. 3302, Fax +86 21 5663 9310 E-Mail shnanshan@hotmail.com

  

Article Information

Received: April 14, 2009
Accepted: November 2, 2009
Published online: December 17, 2009
Number of Print Pages : 11
Number of Figures : 8, Number of Tables : 0, Number of References : 38

  

Publication Details

American Journal of Nephrology

Vol. 31, No. 2, Year 2010 (Cover Date: February 2010)

Journal Editor: Bakris G. (Chicago, Ill.)
ISSN: 0250-8095 (Print), eISSN: 1421-9670 (Online)

For additional information: http://www.karger.com/AJN


Article / Publication Details

First-Page Preview
Abstract of Original Report: Laboratory Investigation

Received: 4/14/2009
Accepted: 11/2/2009
Published online: 12/17/2009
Issue release date: February 2010

Number of Print Pages: 11
Number of Figures: 8
Number of Tables: 0

ISSN: 0250-8095 (Print)
eISSN: 1421-9670 (Online)

For additional information: http://www.karger.com/AJN


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