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Published in: Diabetology & Metabolic Syndrome 1/2014

Open Access 01-12-2014 | Research

Atorvastatin inhibits the expression of RAGE induced by advanced glycation end products on aortas in healthy Sprague–Dawley rats

Authors: Lei Xu, Panpan Zang, Bo Feng, Qiaohui Qian

Published in: Diabetology & Metabolic Syndrome | Issue 1/2014

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Abstract

Background

Atorvastatin can downregulate the expression of receptor for advanced glycation end products (RAGE) in the aortas of diabetic rats. However, its effect on healthy rats remains unclear. The aim of this study was to observe the direct impact of atorvastatin on advanced glycation end products- (AGEs) induced RAGE expression in healthy Sprague Dawley (SD) rats.

Methods

SD rats received AGE-BSA (20 mg/kg/day or 40 mg/kg/day), dual treatment (AGE-BSA 40 mg/kg/day and atorvastatin 20 mg/kg/day) or no treatment for 12 and 24 weeks, respectively. The deposition of AGEs and expression of RAGE in the animals’ aortas were assessed by Quantitative RT-PCR, immunohistochemistry, and western-blot tests. Serum levels of AGEs were measured using ELISA.

Results

AGE-BSA upregulated the serum level of AGEs, deposition of AGEs, and expression of RAGE in aortas in a time- and dose-dependent way that can accelerate the development and progression of atherosclerosis. These upregulations could be significantly attenuated by atorvastatin in the absence of its lipid-lowering effects. These data provide further evidence for the novo mechanism of atorvastatin’s pleiotropic effect.

Conclusion

Atorvastatin has a direct inhibitory effect on AGEs-RAGE expression in healthy SD rats. These potential pleiotropic vasculoprotective effects are independent of effects on glucose and lipid control.
Appendix
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Metadata
Title
Atorvastatin inhibits the expression of RAGE induced by advanced glycation end products on aortas in healthy Sprague–Dawley rats
Authors
Lei Xu
Panpan Zang
Bo Feng
Qiaohui Qian
Publication date
01-12-2014
Publisher
BioMed Central
Published in
Diabetology & Metabolic Syndrome / Issue 1/2014
Electronic ISSN: 1758-5996
DOI
https://doi.org/10.1186/1758-5996-6-102

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