雌、孕激素作用后小鼠子宫内膜细胞中核因子-κB的表达

目的　探讨不同浓度雌、孕激素对小鼠子宫内膜细胞核因子 κB(NF κB)表达的影响。　方法　采用去势雌性昆明小鼠模型 ,分为假手术、雌激素、孕激素及雌、孕激素联合组 ,采用免疫组织化学方法检测给药后小鼠子宫内膜NF κB的表达。　结果　雌激素浓度为 30及 10 0 μg·kg-1·d-1时均可促进小鼠子宫内膜细胞NF κB的表达 (P <0 .0 1) ,但无明显的量效相关性 (P >0 .0 5 )。单用孕激素降低子宫内膜细胞胞浆中NF κB的表达 (P <0 .0 1)。雌、孕激素联合促进细胞浆及细胞核的NF κB表达 (P <0 .0 1)。　结论　雌激素可上调小鼠子宫内膜细胞NF κB的表达 ,而孕激素对其表达呈降调节作用 ;NF κB途径可能参与了雌、孕激素对子宫内膜容受性建立的调节

The expression of nuclear factor-kappa-B in murine endometrium after treated with estrogen and progesterone

Objective: To investigate the effect of estrogen and progesterone on murine endometrial nuclear factor kappa B (NF κB)expression, which may be involved in the receptivity establishment. Methods:Ovariectomized mice were randomly divided into control and treatment groups. Estrogen in three different concentrations (10 μg·kg -1 ·d -1 ,30 μg·kg -1 ·d -1 , 100 μg·kg -1 ·d -1 ) was given to three groups for one week; progesterone 2 mg/d was given to one group for three days; three different regimens (different concentrations of estrogen combined with progesterone 2 mg/d×3 d)were given to three groups respectively for one week. Medicine was administered subcutaneously. Control group subdivided into sham group and the group treated with solvent injection only. Twenty four hours after the last treatment, mice were sacrificed, then we took the uterus and analyzed the expression of NF κB by immunohistochemical method. Results: Estrogen at concentrations of 30 μg·kg -1 ·d -1 and 100 μg·kg -1 ·d -1 can significantly stimulate the expression of NF κB in murine endometrial cells ( P <0.01), however they did not exhibit a dose dependent effect ( P >0.05). Progesterone alone can reduce the expression of NF κB in cytoplasma of murine endometrial cells ( P <0.01). Estrogen combined with progesterone can increase NF κB expression both in cytoplasma and in nucleus ( P <0.01). Conclusion: Estrogen can up regulate the expression of NF κB in murine endometrial cells, while progesterone shows down regulation on that. NF κB may be take part in the modulation of estrogen and progesterone on endometrial receptivity establishment.