Dicaffeoylquinic acids in Yerba mate (Ilex paraguariensis St. Hilaire) inhibit NF-κB nucleus translocation in macrophages and induce apoptosis by activating caspases-8 and -3 in human colon cancer cells - PubMed (original) (raw)

. 2011 Oct;55(10):1509-22.

doi: 10.1002/mnfr.201100128. Epub 2011 Jun 8.

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Dicaffeoylquinic acids in Yerba mate (Ilex paraguariensis St. Hilaire) inhibit NF-κB nucleus translocation in macrophages and induce apoptosis by activating caspases-8 and -3 in human colon cancer cells

Sirima Puangpraphant et al. Mol Nutr Food Res. 2011 Oct.

Abstract

Scope: The biological functions of caffeoylquinic acid (CQA) derivatives from various plant sources have been partially elucidated. The objectives were to isolate and purify diCQAs from Yerba mate tea leaves and assess their anti-inflammatory and anti-cancer capabilities in vitro and explore their mechanism of action.

Methods and results: Methanol extracts of dried mate leaves were resolved by flash chromatography and further purified resulting in two fractions one containing 3,4- and 3,5-diCQAs and the other 4,5-diCQA with NMR-confirmed structures. Both fractions inhibited LPS-induced RAW 264.7 macrophage inflammation by suppressing nitric oxide/inducible nitric oxide and prostaglandin E(2) /cyclooxygenase-2 pathways through inhibiting nucleus translocation of Nuclear factor κB subunits, p50 and p65. The diCQA fractions inhibited Human colon cancer cells CRL-2577 (RKO) and HT-29 cell proliferation by inducing apoptosis in a time- and concentration-dependent manner, but did not affect the protein levels of p21, p27, p53, and Bax:Bcl-2 ratio in RKO cells. In HT-29 cells, however, the diCQA fractions increased Bax:Bcl-2 ratio. The diCQA fractions increased the activation of caspase-8 leading to cleavage of caspase-3 in both RKO and HT-29 colon cancer cells.

Conclusion: The results suggest that diCQAs in Yerba mate could be potential anti-cancer agents and could mitigate other diseases also associated with inflammation.

Copyright © 2011 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.

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