Bakuchiol inhibits macrophage-derived foam cell formation by reducing ERK1/2 phosphorylation and upregulating ABCA1 expression
10.20039/j.cnki.1007-3949.2024.09.004
- VernacularTitle:补骨脂酚通过抑制ERK1/2磷酸化并上调ABCA1表达减少巨噬细胞源性泡沫细胞形成
- Author:
Yang WANG
1
;
Qinyi ZHOU
;
Gang WANG
;
Chaoke TANG
Author Information
1. 南华大学衡阳医学院心血管疾病研究所湖南省动脉硬化学重点实验室湖南省动脉硬化性疾病国际科技合作创新基地
- Keywords:
bakuchiol;
foam cell;
ATP-binding cassette transporter A1;
extracellular signal-regulated kinase 1/2
- From:
Chinese Journal of Arteriosclerosis
2024;32(9):763-770
- CountryChina
- Language:Chinese
-
Abstract:
Aim To investigate the impact of bakuchiol(BAK)on lipid accumulation in macrophage-derived foam cell and explore the underlying mechanisms.Methods MTT assay was used to determine the non-toxic concen-tration of BAK on foam cell.Oil red O staining,NBD cholesterol,and Dil-ox-LDL were used to assess lipid accumulation in foam cell.RT-qPCR and Western blot were utilized to measure mRNA and protein expression,respectively.Re-sults BAK promoted cholesterol effux and reduced lipid accumulation in foam cell.BAK upregulated the mRNA and protein expression levels of ATP-binding cassette transporter A1(ABCA1)and concurrently downregulated the phosphoryl-ation levels of extracellular signal-regulated kinase 1/2(ERK1/2).Treatment with the ERK1/2 activator Ro 67-7476 re-sulted in decreased ABCA1 protein expression compared with the BAK-treated group.Conclusion BAK reduced lipid accumulation in foam cell by inhibiting ERK1/2 phosphorylation,upregulating ABCA1 expression,and promoting choles-terol efflux,thereby suppressing foam cell formation.
