Huxin Formula Inhibits Oxidized low-Density Lipoprotein-Induced Foam Cell Formation in THP-1 Macrophages via the LOX-1/NF-κB Pathway

THP1细胞系 泡沫电池 化学 NF-κB 低密度脂蛋白 巨噬细胞 细胞 细胞生物学 脂蛋白 信号转导 生物化学 细胞培养 胆固醇 生物 体外 遗传学
作者
Qiaohuang Zeng,Xiaomin Ou,Jun Cai,Tao-Hua Lan,Weihui Lu,Wei Jiang
出处
期刊:Natural Product Communications [SAGE]
卷期号:19 (9)
标识
DOI:10.1177/1934578x241282836
摘要

Background Macrophage-derived foam cells are essential in the progression of atherosclerosis (AS). Based on our previous study, the Huxin Formula (HXF), a traditional Chinese medicine formula, demonstrates potential in anti-atherosclerosis. Nevertheless, it is still unknown how HXF affects the formation of foam cells derived from THP-1 macrophages. Purpose This research aims to examine the preventive role of HXF in the development of foam cells and its underlying molecular mechanism. Methods THP-1 derived macrophages and THP-1 cells overexpressing LOX-1 (LV-OLR1) were exposed to ox-LDL to establish foam cell models, and then treated with HXF. Meantime, Oil red O staining was used to detect lipid droplet production. ELISA kit was performed to measure intracellular levels of IL-6 and TGF-β. RT-qPCR and Western Blot were then utilized to determine the LOX-1 and NF-κB mRNA/protein levels. Results The findings indicated that HXF treatment potently reduced the lipid accumulation, downregulated IL-6 levels and upregulated TGF-β levels. However, this impact was almost reversed when LOX-1 was overexpressed in THP-1 cells stimulated with ox-LDL. Moreover, THP-1 were treated with HXF markedly reduced the levels of LOX-1 and NF-κB mRNA/protein, whereas overexpressing LOX-1 significantly reversed this effect. Conclusion HXF reduced the formation of foam cell in ox-LDL-stimulated THP-1 macrophages via inhibiting lipid accumulation and inflammation through regulating the LOX-1/ NF-κB pathway. These present findings further indicate a potential beneficial role of HXF in ameliorating atherosclerosis and foam cell formation, while provide a novel potential therapeutic strategy for preventing atherosclerosis.
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