Equol, a Metabolite of Daidzein, Inhibits IgE-Dependent Basophil Activation by Modulating Intracellular Signaling

Currently, the health-promoting effects of equol, an active metabolite of the naturally occurring isoflavone daidzein, in human digestive organs are attracting attention. Although the anti-inflammatory properties of equol have been elucidated and reported, the effect of equol on basophil activation associated with allergy induction has not been clarified.

In this study, we investigated the inhibitory effects of equol on basophil degranulation, which is responsible for anaphylaxis and allergic symptoms.

The rat basophilic leukemia cell line, RBL2H3, was sensitized with anti-ovalbumin IgE and stimulated with ovalbumin in the presence or absence of equol, daidzein, and genistein. β-hexosaminidase and interleukin-4 releases in parallel with phosphorylation of intracellular signaling molecules such as ERK, JNK, p38, and Akt were measured. In addition, the effect of equol on the increase in surface CD63 expression of mouse primary spleen basophils (CD200R3⁺CD49b⁺) was examined following various stimulations including anti-IgE stimulation.

Pretreatment of equol for 15 min significantly inhibited β-hexosaminidase at 20 min and interleukin-4 release at 4 h after stimulation without affecting cell viability. The inhibitory effect of equol on cell degranulation was comparable to that of genistein and daidzein. Treatment with equol also diminished the IgE-dependent increase in the phosphorylation levels of Akt, ERK, JNK and p38. Moreover, equol attenuated IgE-dependent mouse primary basophil degranulation, as indicated by increased CD63 expression. Ionomycin- or thapsigargin-induced CD63 expression was also inhibited by the compound.

These results suggest that equol might be a potential candidate as an anti-allergic agent as well as related isoflavones.