Gossypol and Misoprostol could directly damage the luteal and decidual cells cultured in vitro. The LD50 of gossypol alone to luteal and decidual cells were 1.27±0.09 μg/ml and 3.06±0.23 μg/ml, respectivel...Gossypol and Misoprostol could directly damage the luteal and decidual cells cultured in vitro. The LD50 of gossypol alone to luteal and decidual cells were 1.27±0.09 μg/ml and 3.06±0.23 μg/ml, respectively; however when combined with misoprostol (to luteal cells 5μg/ml, or to decidual cells 10μg/ml), the LD50 of gossypol signifcantly decreased to 0.89±0.25 μg/ml and 1.88±0.26 μg/ml, respectively. The LD50 of misoprostol alone to luteal and decidual cells were 14.29±1.29μg/ml and 24.37±4.49 μg/ml, respectively; but it decreased to 8.79±2.18 μg/mland 17.29±1.56 μg/ml, respectively when combined with gossypol (to luteal cells 0.5 μg/ml, or to decidual cells 1.0 μg/ml), also showing statistical difference. The results suggested that the combination of gossypol with misoprostol had synergistic effect on the degeneration of luteal and decidual cells in vitro.展开更多
The action of Gly-Tyr-NH_2, (GY-NH_2) and Gly-Tyr-LYS(GYK) on ￣(125)I-LH binding, cAMP accumulation and progesterone production was investigated. Incubation of rat luteal cells for 2.5 h with GY-NH_2 and GYK at dosag...The action of Gly-Tyr-NH_2, (GY-NH_2) and Gly-Tyr-LYS(GYK) on ￣(125)I-LH binding, cAMP accumulation and progesterone production was investigated. Incubation of rat luteal cells for 2.5 h with GY-NH_2 and GYK at dosage of 0. 2 mmol/L caused a significant inhidition of basal and gonadotropin-stimulated steroidogenesis. GY-NH_2 and GYK were also found to reduce cAMP formation in response to hCG. The activity of adenylate cycles of luteal cells was inhibitd by 0. 2 mmol/LGY-NH_2 and GYK. GY-NH_2 and GYK at a concentration of 0. 2mmol/L were not found to have an inhibitory effect on 8Br-cAMP-stimulated progesterone preduction. GY-NH_2 and GYK did not affect ￣(125)I-LH binding to LH receptors on the luteal cell surface. These results suggest that GY-NH_2 and GYK inhibit steroidogenesis at the step of gonadotropin-stimulated cAMP formation in luteal cells. Adenylate cyclase in luteal cells was also inhibited.展开更多
Previous work from our laboratory has demonstrated that T lymphocyte-derived cytokine,interferon-gamma(IFN-γ) may play a role in human luteal regression by inhibiting luteal progesterone production.Prostaglandin F2α...Previous work from our laboratory has demonstrated that T lymphocyte-derived cytokine,interferon-gamma(IFN-γ) may play a role in human luteal regression by inhibiting luteal progesterone production.Prostaglandin F2αhas been known as an important luteolytic factor in a wide range of mammalian species.It was of interest to investigate the effects of IFN-γon prostaglandin synthesis and their possible interaction with the inhibition on human luteal steroidogenesis.Human luteal cells were cultured for four days in the presence or absence of IFN-γ.Simultaneously, the productions of progesterone,prostaglandin F2α(PGF2α),Prostaglandin E2(PGE2),and 6-ketoprostaglandin F1α(PGF1α) were evaluated.Concomitant with the inhibition of progesterone production induced by IFN-γ,αbiphasic pattern of response of prostaglandin synthesis was observed,i.e.a slight decrease of PGF2αand PGF1αafterα48 h exposure to IFN-γ while an increase of PGE2 after 96 h. In a separate experiment,a luteotropic action of PGE2 and PGF2a on human luteal cells from different stages was observed during 48 and 96 h periods of culture.In addition,while indomethacin(INDO) treatment markedly blocked the prostaglandin synthesis, the hasal as well as hCG stimulated progesterone production was still inhibited by IFN-γas 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.展开更多
文摘Gossypol and Misoprostol could directly damage the luteal and decidual cells cultured in vitro. The LD50 of gossypol alone to luteal and decidual cells were 1.27±0.09 μg/ml and 3.06±0.23 μg/ml, respectively; however when combined with misoprostol (to luteal cells 5μg/ml, or to decidual cells 10μg/ml), the LD50 of gossypol signifcantly decreased to 0.89±0.25 μg/ml and 1.88±0.26 μg/ml, respectively. The LD50 of misoprostol alone to luteal and decidual cells were 14.29±1.29μg/ml and 24.37±4.49 μg/ml, respectively; but it decreased to 8.79±2.18 μg/mland 17.29±1.56 μg/ml, respectively when combined with gossypol (to luteal cells 0.5 μg/ml, or to decidual cells 1.0 μg/ml), also showing statistical difference. The results suggested that the combination of gossypol with misoprostol had synergistic effect on the degeneration of luteal and decidual cells in vitro.
文摘The action of Gly-Tyr-NH_2, (GY-NH_2) and Gly-Tyr-LYS(GYK) on ￣(125)I-LH binding, cAMP accumulation and progesterone production was investigated. Incubation of rat luteal cells for 2.5 h with GY-NH_2 and GYK at dosage of 0. 2 mmol/L caused a significant inhidition of basal and gonadotropin-stimulated steroidogenesis. GY-NH_2 and GYK were also found to reduce cAMP formation in response to hCG. The activity of adenylate cycles of luteal cells was inhibitd by 0. 2 mmol/LGY-NH_2 and GYK. GY-NH_2 and GYK at a concentration of 0. 2mmol/L were not found to have an inhibitory effect on 8Br-cAMP-stimulated progesterone preduction. GY-NH_2 and GYK did not affect ￣(125)I-LH binding to LH receptors on the luteal cell surface. These results suggest that GY-NH_2 and GYK inhibit steroidogenesis at the step of gonadotropin-stimulated cAMP formation in luteal cells. Adenylate cyclase in luteal cells was also inhibited.
文摘Previous work from our laboratory has demonstrated that T lymphocyte-derived cytokine,interferon-gamma(IFN-γ) may play a role in human luteal regression by inhibiting luteal progesterone production.Prostaglandin F2αhas been known as an important luteolytic factor in a wide range of mammalian species.It was of interest to investigate the effects of IFN-γon prostaglandin synthesis and their possible interaction with the inhibition on human luteal steroidogenesis.Human luteal cells were cultured for four days in the presence or absence of IFN-γ.Simultaneously, the productions of progesterone,prostaglandin F2α(PGF2α),Prostaglandin E2(PGE2),and 6-ketoprostaglandin F1α(PGF1α) were evaluated.Concomitant with the inhibition of progesterone production induced by IFN-γ,αbiphasic pattern of response of prostaglandin synthesis was observed,i.e.a slight decrease of PGF2αand PGF1αafterα48 h exposure to IFN-γ while an increase of PGE2 after 96 h. In a separate experiment,a luteotropic action of PGE2 and PGF2a on human luteal cells from different stages was observed during 48 and 96 h periods of culture.In addition,while indomethacin(INDO) treatment markedly blocked the prostaglandin synthesis, the hasal as well as hCG stimulated progesterone production was still inhibited by IFN-γas 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.
