Abstract: OBJECTIVE It is to observe the influences of Anzi Heji on the JAK/STAT3 signaling pathways on the maternal-fetal interface of anticardiolipin antibody (ACA) positive mice. METHODS Establish ACA positive mice model with humanβ2-GPⅠ as derivant， and administer normal saline to the blank group and humanβ2-GPⅠ to the model group; administer aspirin and high and low dose Anzi Heji respectively to each therapy group， kill the mice at the 15th day of their pregnancy， calculate the embryo resorption rate， and test the ACA of peripheral blood by means of ELISA; test the JAK， GP130 and p-STAT3 of placenta and decidual tissue with immunohistochemical method， and test STAT3 and p-STAT3 with western blot method. RESULTS The embryo resorption rate of the mice of low- and high-dose Anzi Heji groups and aspirin group was lowered obviously， so was the titer of ACA in the serum of mice (P<0.05)， the expression of JAK， GP130 and p-STAT3 on the maternal-fetal interface was raised， and wherein， the expression of JAK， p-STAT3 of placenta had significant difference from that of model group (P<0.05)， and the expression of GP130 and p-STAT3 of decidual tissue had significant difference from that of the model group (P<0.05). CONCLUSION The pathomechanism for ACA to induce pregnancy loss is related to the JAK/ STAT3 signaling pathways on the maternal-fetal interface， and the mechanism for Anzi Heji to produce therapeutic effect is possibly to promote the activation of STAT3 of placenta and decidual tissue by enhancing the expression of JAK of placenta and strengthening the expression of GP130 of decidual tissue.