Casticin, a flavonoid isolated from Vitex rotundifolia, inhibits prolactin release in vivo and in vitro

Aim： To investigate the anti-hyperprolactinemia activity of casticin, a flavonoid isolated from Vitex rotundifolia, and elucidate its molecular mechanism. Methods： Hyperprolactinemia （MIHP） was induced by administration of metoclopramide dihydrochloride （50 mg/kg, tid, ip, for 10 d） in SD rats and t...

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Published in:Acta pharmacologica Sinica 2010-12, Vol.31 (12), p.1564-1568
Main Authors: YE, Qi, ZHANG, Qiao-yan, ZHENG, Cheng-jian, WANG, Yang, QIN, Lu-ping
Format: Article
Language:English
Subjects:
Animals
Cells, Cultured
Dose-Response Relationship, Drug
Estradiol - metabolism
Estrogen Receptor alpha - metabolism
Estrogen Receptor beta - metabolism
Female
Flavonoids - isolation & purification
Flavonoids - pharmacology
Flavonoids - therapeutic use
Fruit - chemistry
Hyperprolactinemia - chemically induced
Hyperprolactinemia - physiopathology
Hyperprolactinemia - prevention & control
Metoclopramide
Original
Phytotherapy
Pituitary Gland - metabolism
Plant Extracts - administration & dosage
Plant Extracts - pharmacology
Plant Extracts - therapeutic use
Prolactin - secretion
Rats
Rats, Sprague-Dawley
Vitex - chemistry
体外释放
催乳素
垂体细胞
类黄酮
雌激素受体α
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Summary:Aim： To investigate the anti-hyperprolactinemia activity of casticin, a flavonoid isolated from Vitex rotundifolia, and elucidate its molecular mechanism. Methods： Hyperprolactinemia （MIHP） was induced by administration of metoclopramide dihydrochloride （50 mg/kg, tid, ip, for 10 d） in SD rats and the primary pituitary cells were prepared from the pituitary glands of the SD rats. Prolactin concentrations were measured using a radioimmunoassay. Cell viability was measured using an MTT assay. The mRNA expression of estrogen receptor alpha and beta in rat pituitary cells was measured using semi-quantitative RT-PCR analysis. Results： The level of serum prolactin in the MIHP model group was 2.1 fold higher than that in the untreated control group （P〈0.01）. Casticin （10, 20, and 40 mg/kg, ip, for 7 d） reduced serum prolactin levels by 33.9%, 54.3%, and 64.7%, respectively （P〈0.01）. The positive control drug bromocriptine 1 mg/kg decreased the serum prolactin concentration in MIHP rats by 44.9%. 1713-Estradiol （E2） significantly increased the proliferation of pituitary cells and casticin （1 and 10 μmol/L） markedly inhibited E2-induced pituitary cell proliferation by 27.7% and 42.1%, respectively. Stimulation of pituitary cells with E2 increased prolactin secretion into the cell culture supernatants, and casticin （0.1, 1, and 10 μmol/L） significantly inhibited the prolactin release stimulated by E2 in a concentration-dependent manner. Casticin （1 and 10 μmol/L） significantly inhibited ERa mRNA expression in pituitary cells stimulated with E2 （P〈O.01） but increased ERI3 mRNA expression at a concentration of 10 μmol/L （P〈0.01）. However, casticin had no effects on proliferation and prolectin release of the unstimulated primary pituitary cells in vitro. Conclusion： Casticin inhibited the release of prolactin from pituitary cells of SD rats stimulated with E2 in vivo and in vitro. These effects might be related with inhibiting the ERα mRNA expression and increasing the ERβ mRNA expression.
ISSN:1671-4083
1745-7254
DOI:10.1038/aps.2010.178