Abstract:

Objective To establish the mouse model of autoimmune-type recurrent spontaneous abortion (RSA), and explore the role of complement in the pathogenesis of autoimmune-type RSA. Methods The mouse model of autoimmune-type RSA was established by intrauterine injection of human β2GP-1 in Balb/c mice (intrauterine injection of β2GP-1 group, n=15), and intrauterine injection of unrelated protein group (n=6), intrauterine injection of adjuvants group (n=13), intrauterine injection of normal saline group (n=10), normal unpregnancy group (n=10) and normal pregnancy group (n=15) were served as controls. The embryo loss rates, mean placental weight, concentrations of complement C3 in peripheral blood and mass concentrations of decay accelerating factor (DAF) in placental tissues were compared among groups. Results The embryo loss rate in intrauterine injection of β2GP-1 group was significantly higher than those in normal pregnancy group and intrauterine injection control groups （P<0.05）. The mean placental weight, concentrations of complement C3 in peripheral blood and mass concentrations of DAF in placental tissues in intrauterine injection of β2GP-1 group were significantly lower than those in normal pregnancy group and intrauterine injection control groups （P<0.05）. Conclusion Intrauterine injection of human β2GP-1 can establish autoimmune-type RSA mouse model. Excessive complement activation may paly an important role in the pathogenesis of autoimmune-type RSA.

Key words: recurrent spontaneous abortion, autoimmune, animal model, β2GP-1, complement C3, decay accelerating factor, mouse