前列腺素和γ干扰素对人黄体细胞甾体激素生成的影响及相互作用

我们以前的工作显示Ｔ－淋巴细胞产生的细胞因子γ干扰素（ＩＦＮ－γ），可能在人黄体退化的过程中，通过抑制黄体孕酮生成而起作用。已知在大多数哺乳类动物中，前列腺素Ｆ２ａ（ＰＧＦ２ａ）是一个重要的溶黄体因子。本工作对γ干扰素与前列腺素的关系作了进一步探讨。实验将人黄体细胞置于有或无γ干扰素的条件下培养４天，同时，测定孕酮、ＰＧＦ２ａ、ＰＧＥ２和６－酮－ＰＧＦ１ａ的生成。伴随着γ干扰素对孕酮合成的抑制，观察到一个前列腺素合成的双相模式反应。即暴露于γ干扰素２４ｈ后，ＰＧＦ２ａ和ＰＧＦ１ａ的合成轻微降低，而培养９６ｈ后ＰＧＥ２的合成增加。在另一实验中，发现ＰＧＥ２和ＰＧＦ２ａ对不同期的人黄体细胞在培养４８ｈ和９６ｈ后均有促黄体作用。此外，在消炎痛显著抑制ＰＧ合成的同时，γ干扰素仍能同样抑制其黄体细胞产生孕酮。这些结果提示：观察到γ干扰素引起的抑制孕酮产生似乎并非由前列腺素造成的，因为在同时加入可以抑制前列腺素合成的消炎痛时，这种抑制效果并不受影响。

Effects and interactions of Prostaglandins and Interferon -γon Steroidogenesis of Human Luteal Cells

Previous work from our laboratory has demonstrated T lymphocyte - derived cytokine, interferon -gamma (IFN -γ) may play a role in human luteal regression by inhibiting luteal progesterone production. Prostagladin F2a has been known as an important luteolytic factor in a widerange of mammalian species. It was of interest to investigate the effects of IFN -γ onprostaglandin synthesis and the possible interaction with the inhibition on human luteal steroidogenesis. Human luteal cells were cultured for four days in the presence or abesence of IFN -γ. Simultaneously, the productions of progesterone, prostaglandin F2a(PGF2a), prostaglandin E2(PGE2),and 6 - keto - prostaglandin F1a(PGF1a) were evaluated. Concomitant with the inhibition of progesterone production induced by IFN -γ, a biphasic pattern of response of prostaglandin synthesis was observed, i. e. a slight decrease of PGF2a and PGF1a after a 48 h exposure to IFN -γ whilean increase of PGE2 after 96 h. In a separate experiment, a luteotropic action of PGE2 and PGF2aon human luteal cells from different stages was observed during 48 and 96 h periods of culture. Inaddition, while indomethacin (INDO) treatment markedly blocked the prostaglandin synthesis, the hasal as well as hCG stimulated progesterone production was still inhibited by IFN -γ as usual. These results suggested that prostaglandins appeared to be not responsible for the observed inhibition of progesterone production since the inhibitory effect was not influenced by concurrent treatment with INDO which suppressed prostaglandin synthesis.