No abstract

A-type procyanidin oligomers in cranberries are known to inhibit the adhesion of uropathogenic bacteria. B-type procyanidin dimers and trimers are absorbed by humans. The absorption of A-type procyanidins from cranberries in humans has not been demonstrated. This study examined the transport of A-type cranberry procyanidin dimers, trimers, and tetramers on differentiated human intestinal epithelial Caco-2 cell monolayers. Procyanidins were extracted from cranberries and purified using chromatographic methods. Fraction I contained predominantly A-type procyanidin dimer A2 [epicatechin-(2-O-7, 4-8)-epicatechin]. Fraction II contained primarily A-type trimers and tetramers, with B-type trimers, A-type pentamers, and A-type hexamers being minor components. Fraction I or II in solution was added onto the apical side of the Caco-2 cell membranes. The media at the basolateral side of the membranes were analyzed using HPLC-MS(n) after 2 h. Data indicated that procyanidin dimer A2 in fraction I and A-type trimers and tetramers in fraction II traversed across Caco-2 cell monolayers with transport ratio of 0.6%, 0.4%, and 0.2%, respectively. This study demonstrated that A-type dimers, trimers, and tetramers were transported across Caco-2 cells at low rates, suggesting that they could be absorbed by humans after cranberry consumption.

Procyanidins, both B-type and A-type can be degraded by human gut microbiota. The microbial metabolites may contribute to the bioactivities of procyanidins.

No abstract

Cranberries are rich source of proanthocyanidins (PAC) that possess plethora health benefits including anti‐proliferative and anti‐inflammatory activities. However, 85% of PAC in Cranberries exist as polymers which cannot be absorbed. Recently, we have developed a depolymerization procedure to convert PAC polymers into absorbable oligomers. The aim of this study was to determine novel functions of depolymerized cranberry proanthocyanidins (dPAC). First, we evaluated the anti‐inflammatory potential of dPAC in primary human adipocytes. Our data showed that dPAC 1) reduced adipose‐derived stem cell differentiation in a dose‐dependent manner, 2) dampened the basal and TNFα‐stimulated pro‐inflammatory gene expressions and 3) inhibited MAP‐kinase ERK and JNK activation. Next, we assessed the anti‐proliferative and apoptotic potentials of dPAC on hepatocellular carcinoma HepG2 cells. Our data showed that dPAC effectively 1) reduced proliferation, 2) increased autophagy and 3) induced paraptosis‐like cell death in HepG2 cells. Collectively, dPAC exerted unique anti‐inflammatory effects in unmodified cells, and anti‐proliferative and pro‐apoptotic effects in modified cancer cells.Grant Funding Source: University of Florida, Institute of Food and Agricultural Sciences