Effects of Apigenin on the Expression of LOX‐1, Bcl‐2, and Bax in Hyperlipidemia Rats

Abstract We aimed to investigate the impact of apigenin on LOX‐1, Bcl‐2, and Bax expression in hyperlipidemia rats and explore the possible molecular pathological mechanism of apigenin in improving hyperlipidemia and preventing atherosclerosis. In hyperlipidemia models, the levels of total cholesterol (TC), triglyceride (TG), low‐density lipoprotein cholesterol (LDL‐c) and the LOX‐1 protein expression were apparently increased ( P< 0.01), while the high‐density lipoprotein cholesterol (HDL‐c) levels and the ratio of Bcl‐2/Bax were reduced significantly ( P< 0.01) in comparison with the standard control group. After the treatment of apigenin, the levels of TC, TG, LDL‐c, and the LOX‐1 protein expression were noticeably decreased ( P< 0.01), while the levels of HDL‐c and the Bcl‐2/Bax ratio were increased ( P< 0.01). The intima was thickened and had protrusions in the hyperlipidemia model group compared to the normal control group. In comparison with the atherosclerosis model group, the degree of aortic lesions in the low‐dose, middle‐dose, high‐dose groups was alleviated. Apigenin can reduce the level of blood lipid, improve hyperlipidemia, and prevent atherosclerosis in hyperlipidemia rats. The molecular mechanism may be related to inhibiting LOX‐1 gene expression and increasing the Bcl‐2/Bax ratio.