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01.12.2014 | Research | Ausgabe 1/2014 Open Access

Diabetology & Metabolic Syndrome 1/2014

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

Diabetology & Metabolic Syndrome > Ausgabe 1/2014
Lei Xu, Panpan Zang, Bo Feng, Qiaohui Qian
Wichtige Hinweise

Electronic supplementary material

The online version of this article (doi:10.​1186/​1758-5996-6-102) contains supplementary material, which is available to authorized users.

Competing interests

The authors declare that they have no competing interests.

Authors’ contributions

LX participated in the design of the study, carried out the immunohistochemistry and drafted the manuscript. PZ carried out the animal experiment, RT-PCR, Western blot and performed the statistical analysis. BF conceived of the study, and participated in its design and coordination and helped to draft the manuscript. QQ participated in preparation of AGEs and Western blot. All authors read and approved the final manuscript.



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.


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.


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.


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.
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