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Enhanced effectiveness of using herbs versus their isolated bioactive compounds in a model of castrate‐resistant prostate cancer
Author(s) -
Zhao Yi,
Huang EChu,
Whelan Jay
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.979.14
Subject(s) - baicalin , berberine , curcumin , herb , apoptosis , chemistry , cell growth , in vitro , pharmacology , cell cycle , traditional medicine , growth inhibition , medicinal herbs , medicine , biochemistry , high performance liquid chromatography , chromatography
Prostate cancer (PCa) is the second most common type of cancer among males in the USA. Bioactive phytonutrients have been shown to have anticancer properties in vitro when isolated from their plant sources; however, their relative effective concentrations are orders of magnitude greater than achievable in humans. As such, is it possible to achieve an effective human equivalent dose by using the herb these compounds were originally derived from or with combinations of herbs or their bioactives? In this study, we investigated the differential effects of the bioactive compounds berberine, baicalin and curcumin and compared their effectiveness to goldthread, skullcap and turmeric, respectively, when used in isolation or in combinations. Proliferation of CWR22Rv1 cells (castrate‐resistant PCa cell line) were tested with each bioactive as compared to their corresponding herbs (and in combination) using the Chou‐Talalay method to assess synergy. In each case, sensitivity for growth inhibition was enhanced with the herb (or when used in combination) versus the single compound. Increased expression of the cell cycle inhibitor p21 and inhibition of bcl‐2 accompanied these results. The results show that herbs and their combination can inhibit cell proliferation at lower doses compared to isolated bioactive compounds by inhibiting cell proliferation and enhancing apoptosis. Supported, in part, by the TN AES.