Effects of rosuvastatin on atherosclerosis and LOX-1, NF-κb p65 expression in the aorta of apoe-deficient mice / 解放军医学杂志

ABSTRACT

Objective To investigate the effects of HMG-CoA reductase inhibitor rosuvastatin on atherosclerosis and lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1), and nuclear factor (NF)-kB p65 expressions in apolipoprotein E (ApoE)-deficient mice. Methods Twenty six-week-old ApoE-deficient male mice were randomly divided into hyperlipidemia model group (n=10) and rosuvastatin group (n=10), and they were fed high-fat diet for 13 weeks. Ten six-week-old C57BL/6J (wild type, WT) male mice were selected as normal control group, and were fed normal diet for 13 weeks. After 13 weeks, blood was drawn from the mice to determine serum levels of total cholesterol (TCH), triglyceride (TG), and low density lipoprotein cholesterol (LDL-C). These mice were sacrificed, and their aortas were obtained and examined with HE staining; Western blotting and RT-PCR were used to analyze LOX-1, NF-kB p65 expression intensity in aorta tissue quantitatively. Results The serum level of TCH, TG and LDL-C in rosuvastatin group were lower than those in hyperlipidemia model group (P<0.05). Pathological observation showed that atherosclerotic lesions of the aortas were aggravated significantly in hyperlipidemia model group but alleviated in rosuvastatin group compared with normal control group. Compared with normal control group, LOX-1, NF-kB p65 protein and mRNA expressions significantly increased in hyperlipidemia model group (P<0.05) and reduced in rosuvastatin group (P<0.05). Conclusions Rosuvastatin may lower blood lipid significantly, alleviate the degree of atherosclerotic lesions, and inhibit LOX-1, NF-kB p65 protein and mRNA expressions in the aortic tissue of ApoE-deficient mice. Its anti-athrosclerosis effect is related to down regulation of LOX-1 and NF-kB p65 expressions.