ABSTRACT
<p><b>OBJECTIVE</b>To investigate the effect of BIX01294 (BIX), a methyltransferase inhibitor, on the migration and decidualization of the stromal cells in mouse uterus.</p><p><b>METHODS</b>Mouse endometrial stromal cells were isolated and cultured from the uterus of pregnant mice on day 3.5 of gestation. The migration and decidualization of mouse endometrial stromal cells treated with BIX at different concentrations were observed with wound healing assay and real-time PCR.</p><p><b>RESULTS</b>The migration distance of mouse endometrial stromal cells increased as the BIX concentration increased within the range below 15 µmol/L. Compared with the control cells, the cells treated with BIX (15 µmol/L) showed significantly increased migration distances, but increasing BIX concentration to 20 µmol/L did not further increase the cell migration distance and began to cause cell death. Compared with the control cells, the BIX-treated stromal cells exhibited significantly down-regulated expression of Ehmt2 mRNA, and 15 µmol/L BIX caused inhibition of decidualization in the stromal cells.</p><p><b>CONCLUSION</b>Within a defined concentration range, BIX promotes the migration and inhibits decidualization of mouse uterine stromal cells by inhibiting the expression of Ehmt2 mRNA.</p>
ABSTRACT
<p><b>OBJECTIVE</b>To detect the expression of FABP7 in the placenta of pregnant mice and in HTR-8/Svneo cells.</p><p><b>METHODS</b>Real-time PCR and immunofluorescence were used to detect FABP7 mRNA and protein expressions in the uterine and placental tissue of pregnant mice at different days of gestation. FABP7 expression was also detected in cultured HTR-8/Svneo cells using immunofluorescence assay. The mice were treated with E, Por their combination for 6 and 24 h and Fabp7 mRNA level in the uterus was detected with real-time PCR.</p><p><b>RESULTS</b>At 7.5-10.5 days of gestation, the pregnant mice showed positive expressions of Fabp7 mRNA in the uterus and placenta, and FABP7 protein was detected in the decidualized cells and trophoblast giant cells. The expressions of FABP7 were detected at both the mRNA and protein levels in cultured HTR-8/Svneo cells. In mice treated with P4 alone or with E+Pfor 6 and 24 h, the expression level of Fabp7 mRNA was upregulated in the uterus. Fabp7 upregulation was observed in mice at 24 h following Etreatment but not at 6 h.</p><p><b>CONCLUSION</b>FABP7 is expressed in trophoblast giant cells and decidual cells in the placental tissue of mice and in cultured HTR-8/Svneo cells, suggesting the involvement of FABP7 in placental development and in maintenance of pregnancy. Eand Pcan regulate the expression of FABP7 in mouse uterus.</p>
ABSTRACT
<p><b>BACKGROUND</b>Excessive reactive oxygen species (ROS) may lead to a number of reproductive diseases such as polycystic ovary syndrome. This study aimed to establish an animal model of ovarian oxidative stress and to assess the protective effect of curcumin against oxidative injury.</p><p><b>METHODS</b>Ovarian oxidative stress was induced in female Kunming mice (n = 40) with intraperitoneal injection of 8 mg/kg sodium arsenite (As) once every other day for 16 days; meanwhile, they were, respectively, treated by intragastric administration of 0, 100, 150, or 200 mg/kg (n = 10/group) curcumin once per day for 21 days. Ten normal mice were used as control. Then, the mice were injected intraperitoneally with BrdU and sacrificed; the right ovaries were collected for hematoxylin and eosin (HE) staining and BrdU immunohistochemistry, and the left ovaries for enzyme-linked immunosorbent assay (ELISA) and Western blotting analyses.</p><p><b>RESULTS</b>The ELISA results showed that ROS (11.74 ± 0.65 IU/mg in 8 mg/kg AS + 0 mg/kg curcumin group vs. 10.71 ± 0.91 IU/mg in control group, P= 0.021) and malondialdehyde (MDA) (0.32 ± 0.02 nmol/g in 8 mg/kg AS + 0 mg/kg curcumin group vs. 0.27 ± 0.02 nmol/g in control group, P= 0.048) increased while superoxide dismutase (SOD) (3.96 ± 0.36 U/mg in 8 mg/kg AS + 0 mg/kg curcumin group vs. 4.51 ± 0.70 U/mg in control group, P= 0.012) and glutathione peroxidase (17.36 ± 1.63 U/g in 8 mg/kg AS + 0 mg/kg curcumin group vs. 18.92 ± 1.80 U/g in control group, P= 0.045) decreased in the ovary after injection of As, indicating successful modeling of oxidative stress. Curcumin treatment could considerably increase SOD (4.57 ± 0.68, 4.49 ± 0.27, and 4.56 ± 0.25 U/mg in 100 mg/kg, 150 mg/kg, and 200 mg/kg curcumin group, respectively, allP < 0.05) while significantly reduce ROS (10.64 ± 1.38, 10.73 ± 0.71, and 10.67 ± 1.38 IU/mg in 100 mg/kg, 150 mg/kg, and 200 mg/kg curcumin group, respectively, allP < 0.05) and MDA (0.28 ± 0.02, 0.25 ± 0.03, and 0.27 ± 0.04 nmol/g in 100 mg/kg, 150 mg/kg, and 200 mg/kg curcumin group, respectively; bothP < 0.05) in the ovary. HE staining and BrdU immunohistochemistry of the ovarian tissues indicated the increased amount of atretic follicles (5.67 ± 0.81, 5.84 ± 0.98, and 5.72 ± 0.84 in 100 mg/kg, 150 mg/kg, and 200 mg/kg curcumin group, respectively, all P < 0.05), and the inhibited proliferation of granular cells under oxidative stress would be reversed by curcumin. Furthermore, the Western blotting of ovarian tissues showed that the p66Shc expression upregulated under oxidative stress would be lowered by curcumin.</p><p><b>CONCLUSION</b>Curcumin could alleviate arsenic-induced ovarian oxidative injury to a certain extent.</p>