Leonurus japonicus,Melia azedarach,Pueraria montana var. lobata,Schisandra chinensis,Solanum lyratum
4H-1-Benzopyran-4-one, 7-hydroxy-3-(4-hydroxyphenyl)-/k251b/K 251-6/Tatoin/Soybean Extract/7-Hydroxy-3-(4-hydroxyphenyl)-4H-chromen-4-one/7-Hydroxy-3-(4-hydroxyphenyl)-4H-1-benzopyran-4-one (7-Hydroxy-3-(4-hydroxyphenyl)chromone/4',7-Dihydroxyisoflavone/Daidzeol/7-Hydroxy-3-(4-hydroxy phenyl) chromone/7,4'-dihydroxyisoflavone/isoaurostatin/Daizeol/Daidzein/Daidsein
Daidzein is a soy isoflavone, which acts as a PPAR activator.
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We compared the effects of two major isoflavones, daidzein and genistein, on lipid metabolism in rats. Daidzein (150 mg/kg diet), genistein (150 mg/kg diet), daidzein and genistein (1:1, 300 mg/kg diet), or control diets were fed to 4 groups of 6-week-old ovariectomized (Ovx) and non-Ovx Sprague Dawley rats for 4 weeks. Dietary daidzein, but not genistein, reduced serum and hepatic total cholesterol levels significantly relative to that by the control group, regardless of whether the rats had undergone ovariectomy. Genistein did not exhibit any physiological effects on lipid levels, but did affect genes involved in cholesterol metabolism. These results indicate that daidzein and genistein may influence lipid regulation via differing modes of action.
ApoB; daidzein; gene expression; hypocholesterolemic effect; ovariectomy
Dietary daidzein, but not genistein, has a hypocholesterolemic effect in non-ovariectomized and ovariectomized female Sprague-Dawley rats on a cholesterol-free diet.
Bhattarai K1, Adhikari S1, Fujitani M1,2, Kishida T1,2.
We previously found that daidzein decreased food intake in female rats. To understand the mechanism of anorectic action of dietary daidzein, it is necessary to determine distributions of daidzein and S-equol, a metabolite of intestinal bacterial conversion from daidzein, in the body. In the present study, we measured the concentrations of daidzein and S-equol in serum and bile in sham-operated and ovariectomized female rats fed a diet containing 150 mg/kg daidzein for 7 days. Dietary daidzein increased serum and bile concentrations of S-equol to far higher levels than those of daidzein. S-equol concentration was more than several hundred fold-higher in bile than in serum, regardless of ovariectomy. Moreover, to investigate whether accumulation of S-equol is facilitated by efficient enterohepatic circulation during continuous intake of daidzein and S-equol, female rats were fed diet containing daidzein or S-equol (both 150 mg/kg), or control diet for 1, 2, 3, or 5 days. Dietary daidzein significantly increased serum and bile concentrations of S-equol in a time-dependent manner, but not those of daidzein. These results indicated that substantial proportion of dietary daidzein was converted to S-equol, which underwent efficient enterohepatic circulation and predominantly accumulated there.
Dietary daidzein induces accumulation of S-equol in enterohepatic circulation to far higher levels than that of daidzein in female rats with and without ovariectomy.
Fujitani M1, Mizushige T2, Bhattarai K1,3, Adhikari S3, Ishikawa J4, Kishida T1,3.
Choriocarcinoma is a highly malignant tumor arising from abnormal gestational trophoblast proliferation. Although chemotherapy has dramatically improved the prognosis, there are still some patients who become drug-resistant or relapse. Daidzein has garnered interest in its antitumor activity especially in proliferation inhibition. However, few reports exist on daidzein effect in growth of choriocarcinoma. Therefore, in this study, we performed in vitro and in vivo experiment in JAR and JEG‑3 to investigate the effect of daidzein in proliferation of choriocarcinoma. Daidzein inhibited cell growth in a time- and dose-dependent way. Cell cycle was arrested at G1 phase and expression of cyclin D1, c-myc, PCNA was reduced while p21 was upregulated during daidzein treatment. At the same time, the expression of p-ERK was downregulated and translocation into nuclear afterwards was also inhibited. Moreover, ERK agonist ceramide C6 abolished daidzein’s effects on cell proliferation. Besides, in vivo experiment also showed daidzein’s anti-proliferation function as xenografts growth was inhibited and expressions of c-myc, PCNA and p-ERK were suppressed. In conclusion, results in our study demonstrate daidzein can inhibit choriocarcinoma cell proliferation in vitro and in vivo; underlying mechanism behind the inhibitory effects may probably be suppressing ERK pathway and afterwards arresting cell cycle at G1 phase.
Daidzein inhibits choriocarcinoma proliferation by arresting cell cycle at G1 phase through suppressing ERK pathway in vitro and in vivo.
Zheng W1, Sun R2, Yang L1, Zeng X1, Xue Y1, An R1.