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Evaluation of herbal products as potential inhibitors of MDR1
Author(s) -
Dresser G. K.,
McDonald W.,
Kim R. B.,
Bailey D. G.
Publication year - 2004
Publication title -
clinical pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.941
H-Index - 188
eISSN - 1532-6535
pISSN - 0009-9236
DOI - 10.1016/j.clpt.2003.11.301
Subject(s) - pharmacology , black cohosh , verapamil , traditional medicine , digoxin , valerian , phytochemical , chemistry , kava , phytotherapy , ginseng , medicine , heart failure , alternative medicine , menopause , organic chemistry , pathology , calcium
Herb‐drug interactions are increasingly noted to be a potentially preventable cause of drug toxicity or loss of therapeutic efficacy. In addition to their effects on CYP enzymes, phytochemicals in St. John's wort and grapefruit juice are reported to interact with the drug efflux transporter, P‐glycoprotein (P‐gp)/MDR1. However, the potential effects of other popular, phytochemical rich herbs on MDR1 function have not been established. Ethanolic extracts of several herbal products were prepared. Bidirectional digoxin transport was determined across polarized Caco‐2 cells containing P‐gp. Herbal extracts were added to apical and basal compartments. Inhibitory effects of the herbal extracts were compared to verapamil 20 uM (positive control) and ethanol 2.5% (negative control). Viability of Caco‐2 monolayer was confirmed by measuring inulin leak. Black Cohosh and St. John's wort were the most potent inhibitors of P‐gp and completely abolished digoxin transport. The effect at 1.25 mg/ml was comparable to that of verapamil 20 uM. Echinacea, Feverfew, and Valerian inhibited digoxin transport by 70–80%. Ginseng and Perilla at similar concentrations did not affect digoxin transport. Kava and Garlic extracts appeared to compromise the integrity of the Caco‐2 monolayer. Additional studies of Black Cohosh, Echinacea, Feverfew and Valerian are needed to determine the potential clinical relevance of these findings. Clinical Pharmacology & Therapeutics (2004) 75 , P79–P79; doi: 10.1016/j.clpt.2003.11.301