Fig 2: Effects of CD200Fc on inflammatory response pathway in KGN cells and vascular permeability-related protein and cell cytoskeleton in HUVECs. (A) The cells were treated with vehicle (Ctrl), and 10 IU/ml hCG with or without 100 ng/ml CD200Fc for 24 h, and the protein levels of CD200, CD200R, Cyp19a1, IL-1β, and TNFα were examined by western blotting. (B) The ovarian expression of NF-κB, p-NF-κB, p38 MAPK, and p-p38 MAPK, and the relative NF-κB and p38 MAPK activity were derived as p-NF-κB and p-p38 MAPK, and are expressed as fold changes over Ctrl. HUVECs were treated with condition culture medium from KGN (10 IU/ml hCG with or without 100 ng/ml CD200Fc) for 24 h. (C) The levels of vasoactive proteins VEGF and VEGFR2, and cell junction proteins Occludin, Claudin 5, and ZO-1 were examined by western blotting. (D) Fluorescent photomicrographs of HUVECs monolayer stained with TRITC-phalloidin with a final concentration of 20 mg/ml. Data were presented as means ± SD, *P < 0.5, **P < 0.01, ***P < 0.001 versus Ctrl.

Fig 3: Effects of hCG on CD200 and inflammatory response pathway in KGN cells and the effects of CM on vascular permeability in HUVECs. The cells were treated with vehicle control (Ctrl) and 1, 10, and 100 IU/mL hCG for 24 h. The protein levels of CD200 and CD200R (A), Cyp19a1, IL-1β, and TNFα (B), and of NF-κB, p-NF-κB, p38 MAPK, and p-p38 MAPK (C) were examined. HUVECs were treated with condition culture medium from KGN for 24 h. (D) The levels of vasoactive proteins VEGF and VEGFR2, and cell junction proteins of Occludin, Claudin 5, and ZO-1 in HUVECs. (E) Fluorescent photomicrographs of HUVEC monolayer stained with TRITC-phalloidin with a final concentration of 20 mg/ml. Data were presented as means ± SD, *P < 0.5, **P < 0.01, ***P < 0.001 versus Ctrl.