Background: Xiang Fu (
Cyperus rotundus
L) enters the liver, spleen and triple warmer meridians, and has qi stagnation-removing,
qi circulation-promoting, menstruation-regulating and pain-relieving effects. Besides, it can improve ovarian function, and
has hypolipidemic, hypoglycemic and neuroprotective actions.
Objectives: To study the biflavone constituents in
Cyperus rotundus L and to investigate the effect and mechanism of amentoflavone
on inhibition of uterine tumors. Modern chromatographic techniques were applied for isolation and purification of
compounds, which were then structurally elucidated based on their physicochemical properties and spectral data.
Methods: Female SD rats were injected with diethylstilbestrol and progesterone to establish the pathological model of uterine
fibroids. The rats were then randomly divided into amentoflavone high-, medium- and low-dose groups, mifepristone group,
model group and blank control group (n=10 in each group), and these administered for six consecutive weeks. 24 h after the last
administration, the rats were sacrificed, changes in uterine coefficient were observed, and morphological features of apoptotic
cells in uterine smooth muscle tissues were detected. Afterwards, serum estradiol and progesterone levels were determined by
radioimmunoassay, as well as NOS level in uterine fibroid tissue homogenates. Pro- and anti-apoptotic genes Bcl-2 and Bax were
determined by immunohistochemical assay.
Results: Four biflavone constituents were isolated and obtained. Amentoflavone could markedly reduce the uterine coefficient
in model rats, lower serum estrogen levels in rats with uterine fibroids, improve the pathological conditions of uterine tissues,
markedly reduce the number of Bcl-2- and Bax-positive dots in smooth muscles, and significantly inhibit the tumor-like proliferation
in model rats (P<0.01), which were most obvious in the amentoflavone high-dose group.
Conclusion: It concludes that amentoflavone has a significant inhibitory effect on uterine tumors in rats. Its mechanism may
be by elevating Bax protein expression, down-regulating Bcl-2 expression, forming homodimers Bax/Bax, and reducing plasma
estradiol and progesterone to promote apoptosis of uterine fibroid cells.
