Effect of prostaglandin E2 on rate of decidualization in rats.

Based on morphology, it has been suggested that prostaglandin E2 (PGE2) accelerates the process of endometrial stromal cell differentiation to decidual cells in the rat. The present study investigated this possibility, using changes in uterine weight and in endometrial alkaline phosphatase (ALP) activity as indicators of decidualization. Rats were ovariectomized and treated with one of two steroid protocols; the first was identical to that previously used for the study of morphology, the second a modified protocol which results in greater uterine sensitization for decidualization, producing larger amounts of decidual tissue, thereby making it easier to detect differences between treatments. On the day of uterine sensitization, rats within each treatment protocol were given a unilateral intrauterine infusion of phosphate-buffered saline (PBS) or PGE2 plus indomethacin, and killed 24, 48 or 72 h later. The time-courses for the increases in uterine weight and ALP activity in uterine horns infused with PBS or PGE2 plus indomethacin differed between steroid protocols, but within a protocol were statistically indistinguishable. The results do not support the hypothesis that PGE2 accelerates the process of decidualization but do provide additional support for the notion that PGE2 is a physiological rather than pharmacological mediator of decidualization.