ASSA13-03-11 Both Atorvastatin and Fenofibrate Down-Regulate CXCL16 Expression in ApoE Knockout Mice

Objective CXCL16 plays an important role in atherogenesis. It participates in several processes of atherosclerosis, including chemoattracting actived T cells, promoting cell – cell adhesion and acting as a scavenger receptor. CXCR6 is known as the specific receptor of CXCL16. The aim of this study is to investigate effects of Atorvastatin and Fenofibrate on atherosclerosis and CXCL16 expression in ApoE Knockout Mice. Methods ApoE knockout mice were divided into three groups, including atorvastatin group, fenofibrate group and control group. After 8 weeks feeding with a “Western” diet, all mice were euthanized. Aorta paraffin sections were performed HE stain to observe and analyse atherosclerotic lesion. Expressions of CXCL16 and CXCR6 were detected by immunohistochemistry and quantitative analysed using digital quantitative analysis software. Real-Time PCR was used to quantify CXCL16 mRNA expression. Results The atherosclerotic lesion were alleviated in Atorvastatin and Fenofibrate group than that in control, the ratio of area of plaque to area of vessel lumen were significantly deceased (0.1684 ± 0.1449 and 0.1677 ± 0.1450 vs. 0.4241 ± 0.2654 P < 0.05). The expression of CXCL16 and CXCR6 inaorta was alleviated in Atorvastatin group and Fenofibrate group compared with control. CXCL16 mRNA expression was significantly decreased in Fenofibrate group (0.767 ± 0.819 vs. 1.00 ± 0.996 P < 0.05), but not in Atorvastatin group compared with control (0.222 ± 0.189 vs 1.00 ± 0.996). Conclusion Both Atorvastatin and Fenofibrate attenuated atherosclerosis and down-regulated CXCL16 protein in ApoE knockout mice. CXCL16 mRNA expression was inhibited by Fenofibrate but not by Atorvastatin. Down-regulating CXCL16 protein could be one way of decreasing atherosclerosis by Atorvastatin and Fenofibrate, but via different mechanisms.