Tectoridin, an isoflavone isolated from Maackia amurensis, is a phytoestrogen and activates estrogen and thyroid hormone receptors. Tectoridin exerts the estrogenic effects via ER-dependent genomic pathway and GPR30-dependent nongenomic pathway[3]. Tectoridin scarcely binds to ER alpha as compared to 17beta-estradiol and genistein. Despite poor binding to ER alpha, tectoridin induced potent estrogenic effects, namely recovery of the population of cells in the S-phase after serum starvation, transactivation of the estrogen response element, and induction of MCF-7 cell proliferation. The tectoridin-induced estrogenic effect was severely abrogated by treatment with U0126, a specific MEK1/2 inhibitor. Tectoridin promoted phosphorylation of ERK1/2, but did not affect phosphorylation of ER alpha at Ser(118). It also increased cellular accumulation of cAMP, a hallmark of GPR30-mediated estrogen signaling[4]. When tectorigenin at a dose of 50 mg/kg was intraperitoneally administered to mice injured by tert-butyl hyperoxide (t-BHP), it significantly inhibited the increase the activities of plasma ALT and AST by 39% and 41%, respectively, in the t-BHP -treated group. The inhibitory effect of tectorigenin is much more potent than that of a commercially available dimethyl diphenyl bicarboxylate. Orally administered tectoridin showed hepatoprotective activity[5]. The radical scavenging activity of tectorigenin protected the viability of Chinese hamster lung fibroblast (V79-4) cells exposed to hydrogen peroxide (H2O2) via activation of extracellular signal regulated kinase (ERK) pathway. Furthermore, tectorigenin reduced the apoptotic cells formation and cell cycle arrest at G2/M phase induced by H2O2. Tectorigenin increased the activities of cellular antioxidant enzymes like superoxide dismutase, catalase, glutathione peroxidase, and also increased their protein level[6].
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