Regulatory Effect of Bushen Antai Recipe on the Secretion Function and HLA-G Expression of Human Extravillous Cytotrophoblasts HTR-8

OBJECTIVE To study the effects of Bushen Antai Recipe (BAR) on the secretion function and HLA-G expression of human extravillous cytotrophoblasts HTR-8. METHODS SD female rats were treated with BAR or normal saline to prepare for BAR-containing serum or control serum. After centrifugation of the serum， HTR-8 were randomly divided into 4 groups： control group， low-dose BAR (BAR-L) group， medium dose BAR (BAR-M) group and high dose BAR (BAR-H) group. The BAR-L， BAR-M and BAR-H group were treated with 5%， 10% or 20% BAR-containing serum， respectively. The supematants were harvested at 24 h of the culture， and then the levels of hormone， including E₂ (estradiol)， progesterone (P) and human chorionic gonadotropin (HCG)， and regulatory factors of Helper T cells (Th)， including interleukin -4 (IL-4) and interferon gamma (IFN-γ)， were measured by ELISA in culture supernatant. The mRNA of HLA-G was analyzed using quantitative RT-PCR. RESULTS The BAR-L group could promote the secretion of E₂ and P with no statistically significant difference， the BAR-M group and BAR-H group could effectively improve the secretion of E₂ and P， and the BAR-H group is higher than the BAR-M group（P<0.05）.The three groups could improve the HCG secretion effectively（P<0.05），while there were no significant difference among them（P>0.05）. The BAR-L group could promote the secretion of IL-4 with no statistically significant difference（P>0.05）.The BAR-M group and BAR-H group could effectively improve the IL-4 secretion， while there were no significant difference between them（P>0.05）. And the three groups could down-regulate the IFN-γ secretion effectively（P<0.05）. The BAR-M group and high dose group could improve the HLA-G expression effectively（P<0.05)， and the BAR-H group is higher than the BAR-M group（P<0.05）. CONCLUSION The BAR could elevate the secretion in human extravillous cytotrophoblasts and result in the bias response for Th2 type cytokine at the maternal-fetal interface， which might be partially achieved through up-regulating HLA-G expression.