3-(4-Hydroxyphenyl)propionic acid, a major microbial metabolite of procyanidin A2, shows similar suppression of macrophage foam cell formation as its parent molecule

Yu-Ying Zhang; Xiao-Le Li; Tong-Yun Li; Mei-Ying Li; Ri-Ming Huang; Wu Li; Rui-Li Yang

doi:10.1039/c7ra13729j

3-(4-Hydroxyphenyl)propionic acid, a major microbial metabolite of procyanidin A2, shows similar suppression of macrophage foam cell formation as its parent molecule

RSC Adv. 2018 Feb 7;8(12):6242-6250. doi: 10.1039/c7ra13729j. eCollection 2018 Feb 6.

Authors

Yu-Ying Zhang¹, Xiao-Le Li², Tong-Yun Li¹, Mei-Ying Li¹, Ri-Ming Huang¹, Wu Li², Rui-Li Yang¹

Affiliations

¹ Guangdong Provincial Key Laboratory of Food Quality and Safety, College of Food Science, South China Agricultural University Guangzhou 510642 China rlyang77@scau.edu.cn +86-20-85280270 +86-20-85283448.
² College of Food Science and Technology, Hainan University Haikou 570228 China leewuu@163.com +86-898-66193581 +86-898-66198861.

Abstract

The effect of procyanidin A2 (PCA2) and its major colonic metabolite 3-(4-hydroxyphenyl)propionic acid (HPPA) on the suppression of macrophage foam cell formation, and underlying mechanism, were investigated for the first time. The results showed that 12.5 μg mL^-1 PCA2 and HPPA significantly reduced cellular lipid accumulation and inhibited foam cell formation. HPPA promoted macrophage cholesterol efflux by up-regulating mRNA expressions of ABCA1 and SR-B1, while PCA2 significantly increased SR-B1 and LXR-α mRNA expression levels. Moreover, PCA2 and HPPA significantly lowered the elevated levels of CD36 mRNA expression in ox-LDL-treated macrophage cells. Besides these, the ox-LDL-induced cellular oxidative stress and inflammation was also restricted by PCA2 and HPPA treatment via nuclear factor kappa-B pathways. In conclusion, PCA2 and its major microbial metabolite, HPPA, inhibited the conversion of macrophage into foam cells via regulating cellular lipid metabolism and suppressing cellular oxidative stress and inflammation.