Effects of beta-sitosterol on isolated human non-pregnant uterus in comparison to prostaglandin E2

Background: Beta-sitosterol (beta-sitosterol) is one of the several phytosterols widely studied for its potential to reduce benign prostatic hyperplasia and blood cholesterol levels. Objective: In the present study, the effects of (3-sitosterol on spontaneous and agonist-induced contractions in in vitro nonpregnant human uterus with respect to prostaglandin E-2(PGE(2)) were investigated. Materials and Methods: Myometrial strips, measuring approximately 15 mm x 4 mm x 2 mm, were attained from hysterectomy samples of premenopausal women. Longitudinal muscle strips were mounted on tissue baths, under physiological conditions, to measure their isometric contraction. The effects of cumulative amounts of ji-sitosterol on spontaneous motility in the absence and presence of prazosin, atropine, fulvestran, indomethacin, or thylenediaminetetraacetic acid (EDTA), and on agonist-induced motor activity, were examined. Results: On strips in the follicular phase, both beta-sitosterol (1-100 mu g/ml) and PGE(2) (0.1-10 mu g/ml) increase, in a concentration-dependent manner, muscular basic tonus and amplitude and frequency of spontaneous uterine contractions; whereas on strips obtained during periovulatory phase, beta-sitosterol and PGE(2) cause inhibition of uterine motility. For contractile response, the effective concentrations (Ec(50)) were 47.8 mu g/ml and 5.19 mu g/ml, respectively. Unlike indomethacin, the tissue pretreatment with prazosin, fulvestran, atropine, or ethylenediaminetetraacetic acid did not affect the contractile uterine responses to beta-sitosterol. Furthermore, the beta-sitosterol was able to potentiate the contractile response induced by acetylcholine and vasopressin. Conclusions: These observations suggest that beta-sitosterol may be a useful modulator of the uterine motility during menstrual cycle, facilitating female fertility.