Abstract: Objective To investigate the effect of sodium aescinate on atherosclerosis and antioxidant activity in hyperlipidemia model rats and its mechanism. Methods Seventy-two SD ratswere randomly divided into 6 groups: control group, model group, sodium aescinate 0. 5 mg / kg group、 1 mg / kg、 2 mg / kg groups and atorvastatin calcium 10 mg / kg group. Except for the control group, hyperlipidemia rat model was established in the other five groups. After the corresponding drug treatments were administered to each group, the rats were sacrificed, and myocardial tissue sections were prepared for HE staining. The blood lipids, whole blood viscosity indicators, and oxidative stress indicators were detected by automatic biochemical analyzer, and the atherosclerosis index (AI) and index of HDL-C / TC were calculated. The expression of Keap1-Nrf2 / ARE signalingpathway related proteins in rats were detected by using Western blotting. Results The myocardialfiber arrangement in the sodium aescinate 1 mg / kg and 2 mg / kg groups and the atorvastatin calcium10 mg / kg group were more dispersed than that in the model group, the degree of nuclear lysis anddamage were improved, the levels of TC, TG and LDL-C were decreased, the level of HDL-C wasincreased, the final body weight and AI were decreased, and the value of HDL-C / TC was increased when compared with those in the model group. The whole blood viscosity and the plasma viscosity were decreased, the level of ApoA-I and SOD and GSH-Px were increased, the level ofApoB100 and MDA was decreased, and the protein expression levels of Keap1, NQO1, ARE andp-Nrf-2 / Nrf-2 were significantly increased (P < 0. 05). Conclusion Sodium aescinate can improvemyocardial histopathological injury, regulate dyslipidemia, resist atherosclerosis and inhibit oxidative stress in hyperlipidemia model rats, and its mechanism may be related to the activation of Keap1-Nrf2 / ARE signaling pathway.

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