Exp Clin Endocrinol Diabetes 2015; 123(01): 7-10
DOI: 10.1055/s-0034-1385924
Article
© J. A. Barth Verlag in Georg Thieme Verlag KG Stuttgart · New York

Protective Effects of the Sodium/Calcium Exchanger Inhibitor on Endothelial Dysfunction Induced by High Glucose

D. Liu*
1   Department of Endocrinology, The First Clinical Hospital of Harbin Medical University, Harbin, China
,
K.-Z. Cui*
1   Department of Endocrinology, The First Clinical Hospital of Harbin Medical University, Harbin, China
,
Y.-M. Sun
2   Department of Cardiology, The First Clinical Hospital of Harbin Medical University, Harbin, China
,
J.-W. Liu
1   Department of Endocrinology, The First Clinical Hospital of Harbin Medical University, Harbin, China
,
Y.-B. Li
1   Department of Endocrinology, The First Clinical Hospital of Harbin Medical University, Harbin, China
,
Y. Su
1   Department of Endocrinology, The First Clinical Hospital of Harbin Medical University, Harbin, China
› Author Affiliations
Further Information

Publication History

received 13 May 2014
first decision 25 June 2014

accepted 23 July 2014

Publication Date:
22 August 2014 (online)

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Abstract

This study was designed to investigate the protective effects of KB-R7943, an inhibitor of sodium/calcium exchanger (NCX) on endothelial dysfunction induced by high glucose in endothelial cells. NCX expression, NCX activity and oxidative stress index were determined after endothelial cells were exposed to high glucose in the absence and presence of KB-R7943. Coincubation of endothelial cells with high glucose for 6, 12, 24 and 48 h resulted in a significant decrease in NCX expression, superoxide dismutase (SOD) activity and the release of nitric oxide (NO), and increased NCX activity and malondialdehyde (MDA) production. These effects were abolished by KB-R7943. A similar effect was observed after treatment of endothelial cells with H-7, a protein kinase C (PKC) inhibitor and NADPH oxidase inhibitor (DPI). These results suggest that the sodium/calcium exchanger inhibitor exerts beneficial effects on high glucose-induced endothelial dysfunction, which may be related to PKC signal pathway.

*  These two authors contributed equally to this study.