Pueraria Lobata Flowers Extract inhibits THP-1-derived foam cell formation by acti-vating PPARγ to upregulate the expression of ABCA1
10.20039/j.cnki.1007-3949.2024.05.004
- VernacularTitle:葛花提取物通过激活PPARγ上调ABCA1的表达而抑制THP-1源性泡沫细胞形成
- Author:
Rongrong ZHU
1
;
Mengjiao CHEN
;
Zhenwang ZHAO
;
Jiayi LIU
;
Jianfeng WU
;
Yufei WANG
;
Min ZHANG
Author Information
1. 南华大学心血管疾病研究所 动脉硬化学湖南省重点实验室 湖南省动脉硬化性疾病国际科技创新合作基地南华大学生物信息与医学大数据教研室,湖南省衡阳市 421001
- Keywords:
Pueraria Lobata Flowers Extract;
foam cell;
ATP-binding cassette transporter A1;
peroxisome proliferator-activated receptor γ
- From:
Chinese Journal of Arteriosclerosis
2024;32(5):395-401
- CountryChina
- Language:Chinese
-
Abstract:
Aim To explore the effect of Pueraria Lobata Flowers Extract(PFE)on lipid accumulation in mac-rophage-derived foam cells.Methods The concentration of PFE in THP-1-derived foam cells was screened by MTT,intracellular lipid accumulation was detected by oil red O staining and cholesterol detection kit,intracellular cholesterol ef-flux levels were detected by cholesterol efflux assay kit,RT-qPCR and Western blot were used to analyze mRNA and pro-tein expression.Results PFE significantly reduced lipid accumulation in THP-1-derived foam cells.PFE did not affect the mRNA expression of CD36,scavenger receptor-A Ⅰ(SR-A Ⅰ),sterol regulatory element-binding protein 2(SREBP2),3-hydroxy-3-methylglutaryl-CoA reductase(HMGCR),but it could upregulate the mRNA and protein expres-sion levels of ATP-binding cassette transporter A1(ABCA1)(P＜0.05),and promote the intracellular cholesterol efflux of macrophage-derived foam cells(P＜0.01).PFE could activate the activity of peroxisome proliferator-activated receptor y(PPARγ)(P＜0.01)and upregulate the mRNA and protein expression levels of PPARγ(P＜0.05).Compared with the PFE control group,the expression of PPARγ and ABCA1 proteins decreased and cholesterol efflux decreased after GW9662 treatment(all P＜0.01).Conclusion PFE could significantly prevent the lipid accumulation in THP-1-derived foam cells and inhibit the formation of foam cells by upregulating ABCA1 expression and cholesterol efflux mediated by PPARγ.
