Shoutai Wan treatment upregulates the expression of TNFAIP3 and improves T cell immune tolerance at maternal-fetal interface.

ABSTRACT

Shoutai Wan (STW) is a traditional Chinese medicine formula used to treat various conditions. The objective of this study was to evaluate the impact of STW on the abortion rate in the URSA mouse model and elucidate its underlying molecular mechanisms. Female CBA/J mice were mated with male DBA/2 mice to establish the URSA model. Network pharmacological analysis was employed to investigate the potential molecular mechanisms of STW. Hematoxylin-eosin staining, immunofluorescence, and ELISA were performed to examine placental microenvironmental changes, protein expression related to TNFAIP3 and the NF-κB signaling pathway. Treatment with STW reduced the abortion rate in URSA model mice and improved trophoblast development. TNFAIP3 was identified as a potential target of STW for treating URSA, as STW enhanced TNFAIP3 protein expression while decreasing IL-6 and TNF-α secretion in the placenta. Moreover, STW upregulated TNFAIP3 protein expression and Foxp3 mRNA levels, increased the production of anti-inflammatory cytokines such as IL-10 and TGF-ß1, and decreased p-NF-κB expression in CD4+ cells at the placenta. The findings of this study indicate that STW treatment reduces the abortion rate in the URSA mouse model. These effects are likely mediated by increased TNFAIP3 expression and decreased NF-κB signaling pathway activity at the maternal-fetal interface. These molecular changes may contribute to the regulation of T cell immunity and immune tolerance during pregnancy.