4.6 Article

Three polymethoxyflavones from the peel of Citrus reticulata Chachi inhibits oxidized low-density lipoprotein-induced macrophage-derived foam cell formation

期刊

出版社

FRONTIERS MEDIA SA
DOI: 10.3389/fcvm.2022.924551

关键词

atherosclerosis; polymethoxyflavones; foam cells; inflammation; lipid metabolism

资金

  1. special foundation of Guangzhou Key Laboratory [202002010004]
  2. Pearl River S&T Nova Program of Guangzhou [201806010048]
  3. Special Subject of TCM Science and Technology Research of Guangdong Provincial Hospital of Chinese Medicine [YN2018QJ07, YN2016QJ01]
  4. administration of traditional Chinese Medicine of Guangdong Province [20221311]

向作者/读者索取更多资源

This study investigated the regulatory effects of three polymethoxyflavones on foam cell formation and explored the molecular mechanisms. The results showed that these flavones can alleviate inflammation, inhibit oxidized low-density lipoprotein uptake and foam cell formation, and promote cholesterol efflux mediated by high-density lipoprotein.
Foam cell formation is the hallmark of the development and progression of atherosclerosis. The aim of this study was to investigate the regulatory effects of three polymethoxyflavones (PMFs), namely, tangeretin (TAN), 5,6,7,3 ',4 ',5 '-hexamethoxyflavone (HxMF), and 3,5,6,7,8,3 ',4 '-heptamethoxyflavone (HpMF) on macrophage-derived foam cell formation and to further explore the molecular mechanisms. The RAW264.7 macrophage-derived foam cell model was successfully induced by oxidized low-density lipoprotein (ox-LDL) (80 mu g/ml). It showed that TAN, HxMF, and HpMF alleviated ox-LDL-induced NO release while also inhibiting the expression of IL-1 beta, IL-6, and TNF-alpha in RAW264.7 cells. Uptake of excess ox-LDL was inhibited by TAN, HxMF, and HpMF, resulting in the reduction of its foam cell formation. Moreover, TAN, HxMF, and HpMF promoted HDL-mediated cholesterol efflux. Western blot experiment showed that TAN, HxMF, and HpMF inhibited the expression of scavenger receptor class A type I (SRA1) and cluster of differentiation 36 (CD36), while upregulating peroxisome proliferator-activated receptor gamma (PPAR gamma), liver X receptor alpha (LXR alpha), phospholipid ATP-binding cassette transporter G1 (ABCG1), and scavenger receptor class B type I (SRB1) expression. Together, our findings suggested that PMFs inhibited foam cell formation might inhibit lipid uptake via downregulating SRA1/CD36 expression and promote cholesterol efflux from foam cells via upregulating PPAR gamma/LXR alpha/ABCG1/SRB1 expression. This antiatherosclerotic activity is expected to provide new insights into the development of healthcare uses for PMFs.

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