Objective: To study the protective mechanism of resveratrol on atherosclerosis through regulating stromal interaction molecule 1(STIM1). Method: Atherosclerosis (AS) model was established by high-fat diet after ovariectomy in female apoE-/- mice

and then the mice were divided into normal control group

model group

resveratrol low

middle and high dose groups(50

100

150 mg·kg-1) and estradiol (E2) group. The lipid levels in the serum were detected. The changes of morphology in thoracic aorta were measured by oil Red O staining; the protein expression levels of STIM1

calcium release-activated calcium channel modulator 1(Orai1) and estrogen receptor α (ERα) in thoracic aorta were detected by Western blot; and the STIM1 and Orai1 mRNA expression levels were detected by Real-time PCR. Result: As compared with the normal group

the levels of total cholesterol(CHOL)

triglyceride(TG) and low density lipoprotein cholesterol (LDL-C) were significantly increased

while the level of high density lipoprotein cholesterol (HDL-C) was decreased significantly (P<0.05) in model group; the levels of CHOL

TG and LDL-C were significantly decreased and the content of HDL-C was increased after the administration of resveratrol and estrogen (P<0.05). Oil red O staining showed that in normal control group

the vascular structure was integrated

clear

and the intima was continuous; in model group

the intima was obviously thick

with visible lipid plaques; while after treatment with resveratrol or estrogen

the thickness of intima and lipid plaques were reduced. Western blot and Real-time PCR results showed that as compared with the normal group

STIM1

Orai1 protein and mRNA expression levels were increased in model group model group (P<0.05)

and were decreased after treatment with resveratrol or estrogen (P<0.05). In addition

ERα expression was increased after treatment with resveratrol or estrogen as compared with the model group. Conclusion: Resveratrol could delay the AS by up-regulating ERα

down-regulating the expression of STIM1 and Orai1 and inhibiting Ca2+ influx via SOCE.