Elena Cienfuegos-Jovellanos

Antihypertensive effect of a polyphenol-rich cocoa powder industrially processed to preserve the original flavonoids of the cocoa beans.

A natural flavonoid-enriched cocoa powder, commercially named CocoanOX and developed via a patented industrial process, was characterized and tested for a possible antihypertensive effect. The bioavailability of this polyphenol-rich cocoa powder developed at pilot scale was previously demonstrated in humans. The present results showed that this product was very rich in total procyanidins (128.9 mg/g), especially monomers, dimers, and trimers (54.1 mg/g), and mainly (-)-epicatechin (19.36 mg/g). The effect of a single oral administration of CocoanOX in spontaneously hypertensive rats (SHR) was evaluated at different doses (50, 100, 300, and 600 mg/kg). This product produced a clear antihypertensive effect in these animals, but these doses did not modify the arterial blood pressure in the normotensive Wistar-Kyoto rats. Paradoxically, the maximum effect in the systolic blood pressure (SBP) of SHR was caused by 300 mg/kg of CocoanOX. This dose brought about a decrease in this variable very similar to that caused by 50 mg/kg Captopril. It was also surprising that the maximum effect in the diastolic blood pressure (DBP) was caused by 100 mg/kg CocoanOX. The initial values of DBP and SBP were recovered in SHR, respectively, 24 and 48 h postadministration of the different doses of CocoanOX or Captopril. These results suggest that CocoanOX could be used as a functional ingredient with antihypertensive effect, although it would be also necessary to carry out bioavailability and clinical studies to demonstrate its long-term antihypertensive efficiency in humans.

Inhibition of ulcerative colitis in mice after oral administration of a polyphenol-enriched cocoa extract is mediated by the inhibition of STAT1 and STAT3 phosphorylation in colon cells.

We studied a polyphenol-enriched cocoa extract (PCE) with epicatechin, procyanidin B2, catechin, and procyanidin B1 as the major phenolics for its anti-inflammatory properties against dextran sulfate sodium (DSS)-induced ulcerative colitis (UC) in mice. PCE reduced colon damage, with significant reductions in both the extent and the severity of the inflammation as well as in crypt damage and leukocyte infiltration in the mucosa. Analysis ex vivo showed clear decreases in the production of nitric oxide, cyclooxygenase-2, pSTAT-3, and pSTAT1α, with NF-κB p65 production being slightly reduced. Moreover, NF-κB activation was reduced in RAW 264.7 cells in vitro. In conclusion, the inhibitory effect of PCE on acute UC induced by DSS in mice was attenuated by oral administration of PCE obtained from cocoa. This effect is principally due to the inhibition of transcription factors STAT1 and STAT3 in intestinal cells, with NF-κB inhibition also being implicated.