Research on the effect and mechanism of Shoutai Pill on the expression of aquaporin,thymic stromal lymphopoietin and the related cytokines in a mouse model of spontaneous abortion
Objective To explore the effect and mechanism of Shoutai Pill on the expression of aquaporin(AQP),thymic stromal lymphopoietin(TSLP)and the related cytokines in a mouse model of spontaneous abortion.Methods A total of twenty-four female mice of specific pathogen free grade were randomly divided into normal pregnancy group,abortion model group,Shoutai Pill group and dydrogesterone group,with 6 mice in each group.The normal pregnancy group and abortion model group were treated with pure water by gavage,the Shoutai Pill group was treated with Shoutai Pill by gavage,and the dydrogesterone group was treated with dydrogesterone tablets by gavage.The mice in the four groups were all subjected to hematoxylin and eosin(HE)staining and immunohistochemical staining.The general condition,abortion rate,HE staining condition,AQP,TSLP and forkhead box transcription factor O3(FOXO3)protein expression were compared among the four groups.Results There was no significant difference in the body weight among the four groups(P>0.05).The abortion rates in the abortion model group,Shoutai Pill group and dydrogesterone group were all higher than that in the normal pregnancy group,and the abortion rates in the Shoutai Pill group and dydrogesterone group were lower than that in the abortion model group(P<0.05).AQP in the abortion model group,Shoutai Pill group and dydrogesterone group was higher than that in the normal pregnancy group,and their TSLP and FOXO3 were lower than those in the normal pregnancy group.AQP in the Shoutai Pill group and dydrogesterone group was lower than that in the abortion model group,while their TSLP and FOXO3 were higher than those in the abortion model group(P<0.05).Conclusions Treating the spontaneous abortion mice with Shoutai Pill can significantly reduce the abortion rate,and its mechanism may be related to the down-regulation of AQP and the up-regulation of TSLP and FOXO3.