Effect Of Atorvastatin On TRPC5 Expression In Atherosclerosis Of Apolipoprotein E-knockout Mice

OBJECTIVETo observe the changes of TRPC5 in the aorta vessel smooth muscle cells (VSMCs) of ApoE-/- mice, the effect of atorvastatin interference and to investigate the mechanism of atorvastatin therapy.METHODS1. Building animal models:40 male ApoE-/- mice, six-weeks old, feeding with hyperlipidic diet, were used to establish the atherosclerosis model. The mice were randomly divided into model group and atorvastatin group (n=20 each). The mice of atorvastatin group were lavaged with atorvastatin 20 mg·kg-1·d-1. Meanwhile, the model group received normal saline. The healthy C57BL/6J mice (n=20) with the same age had the same genetic background feeding with ordinary food and served as control group.2. After 14 and 24 weeks, the mice of each group, number 10, were sacrificed. The serum was collected for detecting the lipid levels. Then aortic roots of the heart were taken to make paraffin sections for HE staining, measuring and comparing the relative atherosclerotic plaque area in each section.3. The expression of TRPC5 in VSMCs was examined with immuno-histochemical staining. qRT-PCR was used to detect the expression of TRPC5 in the serum and the thoracoabdominal aorta. RESULTS1. Compared with the model group, blood lipids in atorvastatin group were significantly decreased, what’s more, the formation of plaque under aorta intima also declined.2. There is a significantly higher expression of TRPC5 in the model group of 20-week old and 30-week old, compared with the control group at the same age (P<0.05). TRPC5 expression of the model group at 30-week was higher than that of 20-week model group, but it had no statistical significance.3. Compared with the model group of the same age, the protein and mRNA level of TRPC5 showed descending tendency in the atorvastatin group. Compared with 20-week atorvastatin group, TRPC5 expression of 30-week atorvastatin group declined, and the result had statistical significance.CONCLUSIONAtorvastatin suppresses TRPC5 expression, thus attenuating atherosclerotic development in ApoE-/- mice.