Effect of RU‐486 and Related Compounds on the Proliferation of Cultured Macrophages

C P Roberts, S Parthasarathy, R Gulati, Rita Gulati, Ira Horowitz, I Horowitz, A A Murphy
American journal of reproductive immunology (New York, N.Y. : 1989) · 1995 · vol. 34(4) , pp. 248–256 · doi:10.1111/j.1600-0897.1995.tb00949.x · PMID:8579763 · W2039902350
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RU-486, progesterone, and a RU-486 analog inhibited macrophage proliferation, with RU-486 and progesterone showing synergistic effects, while RU-486 antagonized dexamethasone-stimulated growth.

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Abstract

PROBLEM: Macrophages are implicated in the pathophysiology of endometriosis and are influenced by anti-inflammatory steroids as well as anti-oxidants. METHODS: We tested the effect of RU-486, an antiprogesterone, antiglucocorticoid and an antioxidant, on the proliferation of RAW macrophages. RESULTS: The incorporation of 3H-thymidine was significantly inhibited by both progesterone and RU-486. Progesterone and RU-486, in combination, synergistically inhibited macrophage growth. In contrast, dexamethasone-stimulated growth was antagonized by RU-486 in a dose dependent manner. ZK 112,993 which is structurally related to RU-486 but lacks antioxidant properties, also inhibited thymidine incorporation. The synergistic effect of RU-486 and ZK 112,993 with progesterone implicate a mechanism of action separate from receptor bound antagonists. A cell permeable antioxidant, pyrrolidine dithiocarbamate was very effective in inhibiting the incorporation of 3H-thymidine into cells. CONCLUSIONS: These results suggest novel therapeutic modalities in the management of endometriosis via antiglucocorticoid as well as antioxidant mechanisms.

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Condition tags

endometriosis

MeSH descriptors

Growth Inhibitors Macrophages Mifepristone Antioxidants Antioxidants Cell Division Cell Division Glucocorticoids Glucocorticoids Growth Inhibitors Hormone Antagonists Hormone Antagonists Humans Macrophages Macrophages Macrophages Mifepristone Progesterone Progesterone

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