DrugSt Johns Wort Interactions Mechanism

Primary mechanism of drug-herb interaction involves induction or inhibition of hepatic or intestinal metabolism of drugs by cytochrome P 450 (CYP). Another mechanism of drug-herb interaction involves induction or inhibition of intestinal drug efflux pumps including P-glycoprotein and multiple resistance proteins. Any inhibitory effect of herbs on efflux proteins and CYP may result in increased plasma and tissue concentrations of a drug leading to toxicity. On the other hand, any induction of efflux proteins and CYP may lead to significantly reduced concentrations of a drug in plasma and tissue, thus causing treatment failure (16). CYP3A4 is the most abundant isoenzyme of cytochrome P 450 and is responsible for metabolism of more than 73 drugs and numerous endogenous compounds (17). The active components of St. John's wort induce CYP3A4 and CYP2B6 (18,19). In particular, hyperforin is thought to be responsible for isoenzyme induction through activation of a nuclear steroid/pregnane and xenobiotic receptor (20). St. John's wort also induces P-glycoprotein drug transporter and may reduce efficacy of drugs where hepatic metabolism may not be the major pathway of clearance. The component hypericin may be the active ingredient that modulates P-glycoprotein (21). Based on the reported studies, it can be concluded that St. John's wort induces hepatic and intestinal CYP3A4 and modulates intestinal P-glycoprotein pumps. Therefore, it is likely that St. John's wort will interact with drugs that are metabolized via CYP3A4 and P-glycoprotein pumps. However, not all drugs interact with St. John's wort (22).

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