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- Title
Rosiglitazone attenuates indoxyl sulphate-induced endothelial dysfunction.
- Authors
Chou, Chia‐An; Ng, Hwee‐Yeong; Kuo, Wei‐Hung; Chiou, Ting‐Yu Terry; Pei, Sung‐Nan; Li, Lung‐Chih; Lee, Yueh‐Ting; Lee, Chien‐Te
- Abstract
Indoxyl sulphate is a protein-bound uraemic toxin that has deleterious effects on the cardiovascular system. Rosiglitazone ( RGZ) is an insulin sensitizer used for glycaemic control in type 2 diabetes. Rosiglitazone has been shown to be beneficial for cardiovascular disease because of its pleiotropic effects. Whether RGZ can improve indoxyl sulphate-induced endothelial damage has not been investigated. In the present in vitro study, we examined the effects of RGZ on indoxyl sulphate-induced endothelial injury. Endothelial cells were exposed to RGZ (5 and 10 μmol/L) and then treated with indoxyl sulphate (100 and 1000 μmol/L) for 48 h. Indoxyl sulphate upregulated intracellular cell adhesion molecule-1, vascular cell adhesion molecule-1 and monocyte chemotactic protein-1 expression. Indoxyl sulphate also increased the abundance of NADPH oxidase 4 ( NOX4) and nuclear factor ( NF)- κB. Both extracellular signal-regulated kinase ( ERK) 1/2 and p38 mitogen-activated protein kinase ( MAPK) signalling pathways were activated after 48 h treatment with indoxyl sulphate. Pretreatment of cells with both concentrations of RGZ improved indices of endothelial injury. In addition, RGZ attenuated the increase in NOX4 and NF- κB and prevented the activation of the ERK1/2 and p38 MAPK signalling pathways. We conclude that RGZ ameliorates indoxyl sulphate-induced endothelial injury.
- Subjects
ROSIGLITAZONE; SULFATES; CARDIOVASCULAR system; GLYCEMIC index; ENDOTHELIAL cells; MITOGEN-activated protein kinases
- Publication
Clinical & Experimental Pharmacology & Physiology, 2015, Vol 42, Issue 3, p287
- ISSN
0305-1870
- Publication type
Article
- DOI
10.1111/1440-1681.12351