In our previous study, we found that Shoutai pills could improve the embryo implantation rate as well as the levels of estrogen, progesterone and estrogen receptor in rats with stimulated ovulation. However, the mechanism is not clear. This study was designed to investigate the effect of Shoutai pills on the levels of Th1 and Th2 cytokines in rats with stimulated ovulation and the mechanism. The rat model of stimulated ovulation was established by combined injection of pregnant mare serum gonadotropin (PMSG) and human chorionic gonadotropin (HCG). Then the rats were randomly divided into model group (M), Shoutai pills group (S), progesterone group (P) and normal group (N). All the pregnant rats were treated from the first day. The S and P groups were administrated with gavage of Shoutai pills and injection of progesterone respectively, and N and M groups were given the same volume of normal saline and distilled water respectively. After treatment for 7 days, the animals were executed for serum and uterine tissues. The ELISA method was adopted to detect the contents of Th1 cytokines [interferon-γ (INF-γ), interleukin-2 (IL-2)] and Th2 cytokines (IL-4, IL-6, IL-10). The expression of leukemia inhibitory factor (LIF) and leukemia inhibitory factor receptor (LIFR) was detected by Western blotting and real-time PCR. As compared with N group, the expression levels of IFN-γ and IL-2 in M group were significantly increased, and those of IL-4, IL-6, IL-10, LIF and LIFR were significantly decreased (P<0.05). As compared with M group, the levels of IL-4, IL-6, IL-10, LIF and LIFR in S group were significantly increased (P<0.05), and those of IFN-γ and IL-2 were significantly decreased (P<0.05). It was suggested that Shoutai pills can increase the levels of IL-4, IL-6, IL-10, LIF and LIFR as well as reduce the levels of INF-γ and IL-2 in rats with stimulated ovulation. The Shoutai pills may improve endometrial receptivity and promote embryo implantation by maintaining the balance of Th1/Th2 cytokines.
Keywords: Shoutai pills; Th1/Th2; cytokines; rats.