The present disclosure describes a study of estrogenic activity present in various plant species, selectively inducing some but not all estrogenic responses in the uterus. Prepubertal female rats were treated sequentially with various extracts or decoctions of different plant species or its vehicle, followed 1 h later by treatment with estradiol-17.beta. (E) or its solvent. Uteri were excised under anesthesia and histologically processed for eosinophil quantification and morphometric evaluation of various uterine responses to estrogen, at 6 or 24 h after hormone or vehicle treatment. Besides extracts or decoctions, pure phytoestrogens were also used. Additionally, human mammary cancer cells MCF-7 or MDAMB-231 were cultured in presence of the extract (or decoction), E, both or solvent and cell proliferation was evaluated. Various extracts or decoction displayed selective estrogenic and/or antiestrogenic action for some but not all parameters of estrogen stimulation in the uterus and inhibited growth of human mammary cells in culture or antagonized the estrogen-induced increase in their growth. Present results reveal, for the first time, a dissociation of responses to estrogen by phytoestrogens, suggesting its possible therapeutic application as estrogenic compounds not inducing cell proliferation and reveal the anticancerous effect of some of the extracts with possible therapeutic relevance. The dissociation of responses to estrogen additionally suggest therapeutic applications in estrogen-related diseases (for instance, premenstrual syndrome, endometriosis, etc.); the inhibition of eosinophil degranulation suggest an application in diseases related to eosinophils (hypereosinophilic syndrome, allergic and hypersensitivity diseases).

Tchernitchin; Andres

Gaete; Leonardo

Bustamante; Rodrigo

Universidad de Chile

Pharmaceutical product and analysis model for hormone replacement therapy for women and prevention of some cancers and uterine myomas

To reduce the risk of breast cancer, a drug is periodically administered to young mammals before pregnancy in doses of about 1 microgram to 50 micrograms per kilogram of body weight. The drug: (1) competes with and displaces estradiol 17 beta from the mammary gland cells in an effective manner to prevent the possible formation of DNA-damaging epoxide estradiol metabolites; (2) binds to breast tissue to a greater extent than estradiol 17 beta; (3) induces terminal nonlactation differentiation of the mammary gland; (4) is nontoxic and noncarcinogenic; and (5) preferably does not cause anti-ovulatory activity. The drug is selected from a group of drugs including: (1) 4-OH estradiol; (2) d-equilenin; and (3) 17 alpha ethynyl estriol.

estradiol 17 beta/neoplasms

Pharmaceutical product and analysis model for hormone replacement therapy for women and prevention of some cancers and uterine myomas

Prevention of mammary carcinoma

The most complete medicinal herbs database backed by science