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.

Current Status and Future Perspectives on Therapeutic Potential of Apigenin: Focus on Metabolic-Syndrome-Dependent Organ Dysfunction

“…Xu and collaborators (2021) provided evidence regarding the capacity of intragastric administration of apigenin to significantly ameliorate lipid profile by reducing total cholesterol, triglyceride and LDL cholesterol, and prevent atherosclerosis in hyperlipidaemic rats. Interestingly, apigenin also suppressed LDL oxidation and regulated the expression levels of lectinlike oxidized low-density lipoprotein (LDL) receptor-1 (LOX-1), Bcl-2 and Bax in the aorta of hyperlipidaemic rats, suggesting a promising anti-atherosclerotic role of apigenin in vivo [101].…”

Mechanism of Action of Shenerjiangzhi Formulation on Hyperlipidemia Induced by Consumption of a High-Fat Diet in Rats Using Network Pharmacology and Analyses of the Gut Microbiota

“…They belong to the flavonol class of flavonoids and are present in multiple TCM formulations. These flavonols can improve the metabolism of lipids and glucose and reduce the level of cholesterol and TG in serum ( Chang et al, 2011 ; Sekhon-Loodu et al, 2015 ; Xu et al, 2021 ). Flavonols can also increase the GM abundance and increase the F/B ratio, and their effect on bacteria of the phylum Bacteroides is potent, which may be related to SCFA generation ( Mbikay et al, 2018 ; Wang T. et al, 2020 ).…”

Elucidation of active ingredients and mechanism of action of hawthorn in the prevention and treatment of atherosclerosis

“…The result of “compound–target–pathway” network showed that chrysin, luteolin, apigenin, quercetin, oleanolic acid, and corosolic acid can play a potential role in the prevention and treatment of AS by regulating multiple signal pathways. Apigenin can reduce the levels of cholesterol 7α‐hydroxylase (CYP7A1), HMG‐CoA reductase and low‐density lipoprotein receptor (LDL‐R) in the liver of mice fed with high‐fat diet, ameliorate the dysregulated lipid balance (Zhang, Song, Li, & Jin, 2017), and prevent the initiation and development of AS by regulating the expression of apoptotic gene and LOX‐1 gene (Xu, Li, Du, Wang, & Xiao, 2021). Luteolin decreases oxidized LDL‐induced inflammation by inhibiting activator of transcription 3 and signal transducer in vitro, respectively (Ding, Zheng, Yang, Wang, & Ying, 2019) and modulates HMG‐CoA reductase transcription by decreasing the expression and nuclear translocation of Sterol regulatory element binding protein‐2 (Wong, Lin, & Leung, 2015).…”