Objective: To study the anti-atherosclerosis (AS) mechanism of resveratrol (RES) by regulating store-operated calcium channel (SOCC) induced by transient receptor potential channel protein 1 (TRPC1) and stromal interaction molecule 1 (STIM1). Method: Atherosclerosis model was established with female C57BL/6J mice that were fed with high-fat diet after ovariectomy

and then the mice were divided into control group

model group

low-dose resveratrol group

medium-dose resveratrol group

high-dose resveratrol group(50

100

150 mg·kg-1) and estradiol (E2) group(0.3 mg·kg-1). After 16 weeks

serum was collected

and the lipid level and Ca2+ concentration were detected. The morphological changes were measured by oil red O staining. The protein expressions of TRPC1

STIM1 and endothelial nitric oxide synthase (eNOS) were detected by Western blot and Real-time PCR. The activity of eNOS was measured by enzyme-linked immunosorbent assay(ELISA). Result: Compared with model group

total cholesterol(TC)

triglyceride(TG)

low density lipoprotein(LDL) were decreased

while the high density lipoprotein(HDL) was increased in supplementary high-dose resveratrol or estrogen groups (P<0.05). The pathological changes in the model group were obvious compared with control group

after supplementation with RES or estrogen

the pathological changes were significantly reduced in thoracic aorta. Western blot and Real-time PCR results showed that in model group

the protein expressions of TRPC1 and STIM1 were increased

while the protein expression of eNOS was decreased (P<0.05); in supplementary high-dose resveratrol or estrogen group

these changes were reversed (P<0.05). Conclusion: RES could down-regulate TRPC1 and STIM1 gene and protein expressions

inhibit SOCC-mediated Ca2+ influx

increase eNOS expression and resist atherosclerosis.