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. 2019 Jun 20;197(3):376–386. doi: 10.1111/cei.13313

Figure 2.

Figure 2

(f) In‐vivo antagonistic experiments of mifepristone. Model mice were given progesterone (8 mg/kg/day) + normal saline (NS) (Prog.+NS) or progesterone (8 mg/kg/day) + mifepristone (2 mg/kg/day) (Prog.+Mife.), respectively. Progesterone was daily given to mice from day 0·5 of pregnancy to day 15·5. Mifepristone or NS were added from days 5·5 to 15·5. Mice were euthanized on day 15·5 of pregnancy, fetal resorption rates were calculated (a), decay accelerating factor (DAF) protein levels and C3, interleukin (IL)‐1β, IL‐8 and tumour necrosis factor (TNF)‐α levels tested in enzyme‐linked immunosorbent assays (ELISA) (b). (g) In‐vitro effects of anti‐β2 glycoprotein I (GPI) immunoglobulin (Ig)G on HTR‐8/SVneo cell DAF and CD46 expression. Anti‐β2GPI IgG (60 mg/ml, anti‐β2.IgG) or control IgG (60 μg/ml, Cont.IgG) were separately added to HTR‐8/SVneo cells pre‐exposed to human β2GPI (0·2 mg/ml). Cell DAF and CD46 levels were detected 6 h later; data are presented in (c) and (d). (h) In‐vitro influence of progesterone and mifepristone on HTR‐8/SVneo cells DAF expression. DAF levels (e) in HTR‐8/SVneo cells treated with gradient progesterone concentrations (0, 100, 200, 400 ng/ml). DAF levels (f) in HTR‐8/SVneo cells treated with gradient mifepristone concentrations (0, 25, 50, 100 ng/ml). Experiments performed on at least three independent individual samples; *P < 0·05.