Repeated estradiol benzoate treatment protects against the lordosis-inhibitory effects of restraint and prevents effects of the antiprogestin, RU486

Abstract

The following experiment was designed to test two specific questions: (1) Does the antiprogestin, RU486, reduce emergence of lordosis behavior and/or proceptivity in rats given repeated treatment with 10 μg estradiol benzoate (EB) and/or a single high dose (40 μg) of EB? (2) Does RU486 accentuate the effects of a 5 min restraint experience on sexual behaviors in rats given repeated treatment with estradiol benzoate (EB) and/or a high dose of EB? RU486 was used to determine if a high dose and/or repeated treatment with EB enhanced proceptivity and reduced the response to mild stress through an intracellular progesterone receptor-mediated process. Ovariectomized Fischer rats were injected with a single dose of 10 or 40 μg estradiol benzoate (EB) or received 4 consecutive weeks of treatment with 10 μg EB. Forty-eight hours after the last treatment with EB, rats were injected with 5 mg/kg of the antiprogestin, RU486, or the RU486 vehicle. That afternoon, rats were monitored for sexual behaviors. Sexually-receptive rats were then restrained for 5 min and again tested for sexual behaviors. A separate set of rats received 4 consecutive weeks of 10 μg EB treatment before treatment with a higher (5 mg/rat) dose of RU486. Lordosis to mount ratios, lordosis quality, proceptivity, and resistance were monitored. RU486 had no effect on the emergence of sexual behaviors but did accentuate the lordosis-inhibitory effect of restraint in rats given a single treatment with EB. Rats treated for 4 consecutive weeks with EB showed no effect of restraint and were unaffected by RU486. These findings lead to the suggestion that repeated EB initiates select behavioral effects that are not mimicked by acute EB treatment and that the intracellular progesterone receptor may not be involved.

Investigation of the 12-month efficacy and safety of low-dose mifepristone in the treatment of painful adenomyosis

“…In recent years, adenomyosis clinical studies have found that mifepristone can play a role in inhibiting ovulation and directly affects the progesterone receptor, which prevents the proliferation and differentiation of ectopic endometrium, reducing its growth potential and making it shrink [37,38] . Further experimental studies have found that mifepristone can inhibit ectopic endometrial angiogenesis and simultaneously promote ectopic endometrial apoptosis [20,39] .…”