Objective: To explore the immune pathological mechanism of anticardiolipin antibody (ACA) induced fetal loss and the immune regulation mechanism of Anzi Heji. Method: BALB/c mice were randomly divided into 6 groups: control group

model group

low dose group

middle dose group and high dose group of Anzi Heji

aspirin group. At the first day of pregnancy

distilled water was orally given in control group and model group

while the mice in Anziheji groups were given Anziheji groups at dose of 37.7

75.4

150.8 g·kg-1·d-1 respectively

the mice in aspirin group were given aspirin with 0.019 5 g·g-1·d-1. The administration was given for 14 days

once a day. ACA-IgG injected to pregnant mice by intraperitoneal injection to establish animal model of ACA induced fetal loss on the day 8 and day 12 of pregnancy. The peripheral blood CD4+CD25+FOXP3+Treg cells ratio was detected by flow cytometry; ACA level of mice pregnancy was detected by ELISA; the embryo resorption and fetal development situation were observed. Result: In model group

the peripheral blood CD4+CD25+FOXP3+Treg cells ratio was significantly lower than the control group(2.67±0.51)% vs (9.85±1.77)%(P<0.01); compared with model group

the low and middle dose group of Anzi Heji could increase CD4+CD25+FOXP3+Treg cells ratio significantly(9.47±1.26)%

(7.61±1.07)% vs (2.67±0.51)%

P<0.01

and significantly reduce the titer of ACA (P<0.01)

the low dose group of Anzi Heji was better than the middle dose group of Anzi Heji (P<0.01). The low dose group of Anzi Heji could significantly reduce the resorption rate

and significantly increased fetal weight and placental weight (P<0.05). Conclusion: Pathological mechanism of ACA induced fetal loss is related to decreasing immune cells-CD4+CD25+FOXP3+Treg cells percentage. The immune regulatory mechanism of Anzi Heji on ACA induced fetal loss can be achieved by increasing the CD4+CD25+FOXP3+Treg cells ratio