Endometrial tumor necrosis factor α (TNFα) is a likely mediator of early luteal phase mifepristone-mediated negative effector action on the preimplantation embryo

摘要: Cytokines and growth factors are important mediators of progesterone-regulated endometrial receptivity embryo development. Early luteal phase administration a potent antiprogestin-like mifepristone to the rhesus monkey results in desynchrony, loss viability implantation failure. In present study, (2 mg/kg body weight, s.c.) on day 2 after ovulation resulted significant increase (P < 0.01) level tumor necrosis factor [alpha] (TNF[alpha]) glandular vascular compartments endometrium, secretion luminal fluid 6 monkey. There was an associated lag embryonic development, characterized by delayed mitochondrial maturity, poorly developed junctional complexes, relative absence intra-cytoplasmic filaments high degree intra-cellular degenerative features. Exposure TNF[alpha] (0, 0.5, 5, 50 ng/ml) preimplantation stage mouse embryos vitro showed dose-dependent arrest development at both morula blastocyst stages along with ultra-structural features degeneration similar those observed collected from early mifepristone-treated monkeys. The de novo synthesized released proteins terms trichloroacetic acid precipitable ³⁵S morulae blastocysts marked depression following exposure compared control embryos. Based above observation fact that express receptors for TNF[alpha], we suggest increased levels around time uterine adversely affect