Psoralea corylifolia extract induces vasodilation in rat arteries through both endothelium-dependent and -independent mechanisms involving inhibition of TRPC3 channel activity and elaboration of prostaglandin.

CONTEXT: Fructus Psoralea, Psoralea corylifolia L. (Leguminosae), has been widely used in traditional medicines for the treatment of dermatitis, leukoderma, asthma and osteoporosis.

OBJECTIVES

In this study, we sought to study mechanisms underlying the vasoactive properties of Psoralea corylifolia extract (PCE) and its active ingredients.

MATERIALS AND

METHODS

To study mechanisms underlying the vasoactive properties of PCE prepared by extracting dried seeds of Psoralea corylifolia with 70% ethanol, isometric tension recordings of rat aortic rings and the ionic currents through TRPC3 (transient receptor potential canonical 3) channels were measured with the cumulative concentration (10-600 μg/mL) of PCE or its constituents.

RESULTS

Cumulative treatment with PCE caused the relaxation of pre-contracted aortic rings in the presence and absence of endothelium with EC50 values of 61.27 ± 3.11 and 211.13 ± 18.74 μg/mL, respectively. Pretreatment with inhibitors of nitric oxide (NO) synthase, guanylate cyclase, or cyclooxygenase and pyrazole 3, a selective TRPC3 channel blocker, significantly decreased PCE-induced vasorelaxation (p < 0.01). The PCE constituents, bakuchiol, isobavachalcone, isopsoralen and psoralen, inhibited hTRPC3 currents (inhibited by 40.6 ± 2.7, 27.1 ± 7.9, 35.1 ± 4.8 and 47.4 ± 3.9%, respectively). Furthermore, these constituents significantly relaxed pre-contracted aortic rings (EC50 128.9, 4.5, 32.1 and 114.9 μg/mL, respectively).

DISCUSSION AND

CONCLUSIONS

Taken together, our data indicate that the vasodilatory actions of PCE are dependent on endothelial NO/cGMP and also involved in prostaglandin production. PCE and its active constituents, bakuchiol, isobavachalcone, isopsoralen and psoralen, caused dose-dependent inhibition of TRPC3 channels, indicating that those ingredients attenuate Phe-induced vasoconstriction.