Atorvastatin improves plaque stability in diabetic atherosclerosis through the RAGE pathway.

Abstract

To study the improving effect of atorvastatin on plaque stability in diabetes mellitus (DM) mice complicated with atherosclerosis. Apolipoprotein E (ApoE)-/- mice were used to establish the DM mouse model. Half of the mice received atorvastatin after successful modeling. ApoE-/- and C57BL/6J mice were used as controls. Oil red O staining and Masson staining were performed to detect the lipid and collagen components in mice. Immunohistochemical assay was used to observe the expressions of smooth muscle cell (SMC) and Ly-6c. The expressions of receptor for advanced glycation end products (RAGE), monocyte chemoattractant protein-1 (MCP-1) and nuclear factor-κB (NF-κB) in tissues were detected by Western blotting. Finally, the levels of serum soluble RAGE (sRAGE), advanced glycation end products (AGEs), malondialdehyde (MDA) and reduced glutathione (GSH) in mice were also detected. Atorvastatin reduced the area of atherosclerotic plaque and improved the stability of arterial plaque through reducing lipid deposition, the number of macrophages and SMC, increasing collagen fibers. In mice in atorvastatin group, the levels of serum AGEs and sRAGE were decreased. Moreover, atorvastatin inhibited the downstream pathway of RAGE as well as DM, thus inducing the oxidative stress. Atorvastatin improves plaque stability in diabetic atherosclerosis through the RAGE pathway.