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Involvement of P‐glycoprotein in regulating cellular levels of Ginkgo flavonols: quercetin, kaempferol, and isorhamnetin

Quercetin, kaempferol, and isorhamnetin were the most important flavonoid constituents in extracts from Ginkgo biloba leaves. Transport studies of Ginkgo flavonols were performed in Caco‐2 cell mono‐layers. Their apparent permeability in absorptive and secretion directions was determined, and quercetin, kaempferol and isorhamnetin displayed polarized transport, with the Papp,B‐A being higher than the Papp,A‐B (P < 0.01 for quercetin, P < 0.001 for kaempferol and isorhamnetin, Student's t‐test). Bcap37/MDR1 cells, which were transfected with a P‐glycoprotein (P‐gp) gene construct, were treated with quercetin, kaempferol or isorhamnetin. The concentrations of Ginkgo flavonol in Bcap37/MDR1 cells were lower than those in parent cells (P < 0.05 for quercetin, P < 0.01 for isorhamnetin, Mann‐Whitney U test). The concentrations of the flavonol in transfected cells increased when incubated with the P‐gp inhibitor verapamil (P < 0.05 for kaempferol, Mann‐Whitney U test). A colorometric assay for ATPase activity was applied to the detection of interaction of flavonol with P‐gp. Quercetin and kaempferol inhibited the ATPase activity, and isorhamnetin stimulated the ATPase activity (P < 0.05 for isorhamnetin, Mann Whitney U test). The results indicated that Ginkgo flavonols quercetin, kaempferol and isorhamnetin were substrates of P‐gp. The P‐gp type efflux pump might limit the bioavailability of Ginkgo flavonols.