Journal
RSC ADVANCES
Volume 8, Issue 12, Pages 6242-6250Publisher
ROYAL SOC CHEMISTRY
DOI: 10.1039/c7ra13729j
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Funding
- National Natural Science Foundation of China [31471705]
- Earmarked Fund for China Agriculture Research System [CARS-33]
- Natural Science Foundation of Hainan Province, China [317007]
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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 mu g 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-alpha 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.
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