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KB-R7943 Restores Endothelium-Dependent Relaxation Induced by Advanced Glycosylation End Products in Rat Aorta

KB-R7943 Restores Endothelium-Dependent Relaxation Induced by Advanced Glycosylation End Products in Rat Aorta

Ying Su, Nan Mao, Min Li, Xia Dong, Fan-Zhen Lin, Ying Xu, Yan-Bo Li

J Diabetes Complications. Jan-Feb 2013;27(1):6-10.

PMID: 23021774

Abstract:

Objectives:
The aims of this study were to examine the effects of KB-R7943, an inhibitor of Na(+)/Ca(2+) exchanger, on impaired endothelium-dependent relaxation (EDR) induced by advanced glycosylation end products (AGE) in isolated rat aorta.
Methods:
Both acetylcholine (ACh)-induced EDR and sodium nitroprusside (SNP)-induced endothelium-independent relaxation (EIR) were measured after the rings were exposed to AGE in the absence and presence of KB-R7943.
Results:
Co-incubation of aortic rings with AGE (0.1 g/L) for 24 h resulted in a significant inhibition of EDR, but had no effects on EIR. After incubation of the rings in the co-presence of KB-R7943 (0.1-10 μM) with AGE for 24 h, KB-R7943 (10 μM) significantly attenuated impaired EDR. Superoxide dismutase (200 U/mL) and l-arginine (3mM) could ameliorate the impairment of EDR caused by AGE, whereas d-arginine (3mM) had no effect on EDR. Similarly, AGE decreased superoxide dismutase (SOD) activity and the release of nitric oxide (NO), and increased superoxide anion (O(2)(.-)) production in aortic tissue. KB-R7943 (10 μM) significantly decreased O(2)(.-) production and increased SOD activity and the NO release.
Conclusions:
These results suggest that KB-R7943 attenuated the impairment of EDR elicited by AGE partially through scavenging oxygen free radicals.

Chemicals Related in the Paper:

Catalog Number	Product Name	Structure	CAS Number	Price
ALP182004644	KB-R7943		182004-64-4 (free base)	Price

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