Relationship between Ouabain and Asthenozoospermia

A growing number of researches have shown that ouabain can regulate mammalian sperm function and male reproduction by modulating the sperm motility, capacitation and acrosome reaction in vitro. This study further examined the relationship between ouabain and asthenozoospermia. In this study, the rat was intraperitoneally injected with ouabain at different concentrations（low-dose ouabain group： 12.5 μg/kg body weight per day, and high-dose ouabain group： 25 μg/kg body weight per day） for 30 days to establish the asthenozoospermia model. The sperms from 60 males with normal fertility were incubated with ouabain of gradient concentrations（10-7–10-2mol/L） for 4 h. The sperm motility was evaluated under a microscope. Moreover, the endogenous ouabain（EO） level was determined in seminal plasma of mild or severe asthenozoospermia patients and males with normal fertility by competitive inhibition ELISA. The results showed that the sperm motility was significantly diminished in the rats treated with different concentrations of ouabain. The number of motile sperms（grades a and b） was decreased greatly in a time- and dose-dependent manner in 10-5–10-2mol/L ouabain groups（P0.01）, while no obvious change in sperm motility was observed in 10-7–10-6mol/L groups even for 4-h incubation（P0.05）. Furthermore, the EO level was significantly increased in asthenozoospermia patients as compared with that in males with normal fertility（25.27±1.71 μg/L in mild asthenozoospermia patients, 26.52±1.82 μg/L in severe asthenozoospermia patients, 19.31±1.45 μg/L in normal fertility men）（P0.01）. In conclusion, rat asthenozoospermia was successfully established by intraperitoneal injection of ouabain, and 10-5mol/L ouabain was sufficient enough to inhibit sperm motility in vitro. Moreover, EO, a normal constituent of seminal plasma, was highly expressed in asthenozoospermia males as compared with normal fertility ones.

Postcoital Administration of Asoprisnil Inhibited Embryo Implantation and Disturbed Ultrastructure of Endometrium in Implantation Window in Mice

Asoprisnil, a member of the selective progesterone receptor modulators, exerts high proges- terone receptor selectivity, endometrial targeted advantages and significant anti-implantation effect in rats. The purpose of this study was to confirm the anti-implantation effect of asoprisil, investigate the ultrastructural changes of the peri-implantation endometrium in mice and explore the effect of asoprisnil on endometrial receptivity and its targeted contraceptive proficiency. Post-coitus mice were adminis- tered with different dosages （0.2, 0.1, 0.05 mg·g^-1·day^-1） of asoprisnil from day 1 of pregnancy to day 3. Then 3 animals in each group were killed on day 5 of pregnancy, and uteri were collected to examine the ultrastructural changes of endometria under a transmission electron microscope （TEM）. A total of 80 animals were sacrificed on day 8 of pregnancy, and the uterine horns were examined for the presence or absence of nidation sites and the number of implantation embryos. The results showed that the implan- tation rate and the average number of implantation embryos in asoprisnil groups were statistically sig- nificantly decreased as compared with the vehicle control group （P〈0.05）. The TEM results revealed that, in vehicle control group, the tight junction between the luminal epithelia cells was short and straight, the gap was wide; the luminal epithelia cells were covered with plenty of short, clavate and neatly arranged microvilli; the endometril stromal cells were large with plenty of cytoplasm, and showed significant decidual change; there was more than one nucleus in stromal cells, and the karyotheca was integrity. In low dosage and high dosage asoprisnil groups, the tight junction was longer and more curve than in the vehicle control group; microvilli were uneven and asymmetrically distrib- uted in luminal epithelia; the stromal cells were small and the decidual change was not significant; there were karyopyknosis and karyolysis in stromal cells; there were abnormal thick-wall vessels in the en- dometrium. It was suggested that asoprisnil changed the ultrastructure of the endometrium in implantation window, disturbed the endometrial receptivity and finally resulted in embryo implantation failure.