Abstract: Objective To provide basic theoretical basis of atherosclerosis for the prevention and treatment of cardiovascular and cerebrovascular diseases by detecting the expression level of serum lipids, heat shock protein 70 (HSP70), radical oxygen speciesn (ROS) and oxidized low density lipoprotein (ox-LDL) in rat with heat stress pretreatment. Methods SD rats were randomly divided into control, the AS and H + AS groups. The control group with based diet, the AS and H + AS were treated with intraperitoneal injection a single dose of vitamin D₃ (6×10⁵ U/kg) in the first days of experiment began. Then, every 30 days administration of 1 times, a total of three times administration in the next time combines with high fat diet. During the AS animal modeling, the H + AS group was pretreated with heat stress intervention in every one days until the molding time end. After 14 weeks, draw blood from the common carotid artery, centrifuge, HSP70, ox-LDL and blood lipid were detected by ELISA method, ROS was detected by Fenton method and observe the arterial pathological changes. Results By one-way analysis of variance, in AS group, compared with control group, the levels of TC[(31.87 ±3.79) nmol/L vs. (14.14 ±2.95) nmol/L], TG[(226.00 ±17.09) μmol/L vs. (106.10 ±17.57) μmol/L], LDL[(169.17 ±18.75) μmol/L vs. (96.55 ±13.92) μmol/L], ox-LDL[(26.68 ±3.52) μg/L vs. (9.92 ±3.10) μg/L] increase (P<0.05), the arrangement of endothelial cells was in disorder, foam cells were observed and typical atherosclerosis developed. In H + AS group, compared with AS group, the levels of TC[(28.30 ±2.99) mmol/L vs. (31.87 ±3.79) mmol/L] decreased (P<0.05), TG[(168.68 ±26.17) μmol/L vs. (226.00 ±17.09) μmol/L] and LDL[(137.47 ±16.30) μmol/L vs. (169.17 ±18.75) μmol/L] decreased (P<0.01), HSP70[(673.39 ±130.93) ng/L vs. (324.96 ±57.34) ng/L]increased significantly (P<0.01), but ROS is also increased (P<0.01), calcium salts accumulated in the arterial endarterium, but typical atherosclerosis plaques were barely found. Conclusion The method of heat stress intervention can inhibit the formation of atherosclerotic plaque in rats which may be related to the protective effect of HSP70 in the pathogenesis of the disease.