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BackgroundDi(2-ethylhexyl) phthalate (DEHP) exposure reduces embryo implantations, increases embryonic loss, and decreases fetal body weights. However, whether it is associated with the alteration of luteal function remains unknown. Thus, our aim in this study was to explore the effect and mechanism of DEHP on luteal function in pregnant mice in vivo.MethodsMice were administered DEHP by gavage at 125, 250, 500 mg/kg/day from gestational days (GD) 1 to 9 or 13. Levels of serum progesterone and estradiol were measured by radioimmunoassay. The numbers and sizes of corpora lutea were calculated by ovarian histomorphology. Steroidogenic enzymes were assessed by qRT-PCR. CD31 protein was detected by immunocytochemistry, and prostaglandin F2alpha (PGF2alpha) levels were evaluated by enzyme immunoassay.ResultsTreatment with DEHP significantly inhibited progesterone secretion in pregnant mice in a dose-dependent manner but did not inhibit estradiol production on GD 9 and 13. Treatment also showed concomitant decreases in transcript levels for key steroidogenic enzymes (CYP11A, 3β-HSD, and StAR) on GD 13. Furthermore, DEHP administration significantly reduced the numbers and sizes of corpora lutea on GD 13. No significant changes in the ratio of ovary weight vs. body weight were observed between the control group and treated animals on GD 9 and 13. In addition, treatment with DEHP significantly inhibited CD31 expression of corpora lutea, whereas plasma PGF2alpha levels in DEHP treatment groups were significantly higher compared with the control groups on GD 9 and 13.ConclusionsThe results show DEHP significantly inhibits luteal function of pregnant mice in vivo, with a mechanism that seems to involve the down-regulation of progesterone and steroidogenic enzymes message RNA, the decrease in CD31 expression, and the increase in PGF2alpha secretion.Electronic supplementary materialThe online version of this article (doi:10.1186/s12958-015-0013-4) contains supplementary material, which is available to authorized users.

The androgen receptor (AR) is a ligand-activated transcription factor that is important for both the male and female reproductive systems. The expression and regulation of AR in the uterine endometrium during early pregnancy and decidualization remain relatively under-investigated, so we sought to immunohistochemically examine the spatiotemporal expression of AR in mouse uteri during the peri-implantation period as well as in response to specific steroid hormones. AR protein was found in the nuclei of uterine stromal cells starting on pregnancy Days 1 and 2, with its abundance increasing on Days 3 and 4. From pregnancy Days 5 to 9, however, the expression of AR markedly declined in stromal zones of uteri. No signal was detected in the decidualized cells surrounding the site of embryo implantation; moreover, no AR immunostaining was observed in decidualized uterine cells in an artificial oil-induced model of decidualization. Progesterone significantly inhibited AR protein expression, whereas estrogen dramatically elevated AR abundance in the stroma of ovariectomized mouse uteri. Taken together, our results are the first to demonstrate that decidualization and progesterone significantly inhibited the AR protein expression in vivo, whereas estrogen increased AR protein levels in the stromal cells of mouse uteri. These responses might be advantageous for the proliferation and differentiation of uterine stroma and for embryo implantation during early pregnancy.

Expression and function of the follicle‑stimulating hormone receptor (FSHR) are traditionally thought to be limited to the ovary in females. However, recent studies have indicated that the FSHR is also expressed in endothelial cells of the placental vasculature, and that the haploinsufficiency of the feto‑placental FSHR impaired the growth of the mouse placenta. The aim of the current study was to investigate the placental expression of FSH and FSHR in pregnancies complicated by pre‑eclampsia. Placental tissue samples were collected from 20 pregnancies with pre‑eclampsia and 25 normal pregnancies. Placental FSH and FSHR mRNA levels were measured by reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR), while FSH, FSHR and CD31 protein expression were examined by immunohistochemistry. Additionally, levels of serum FSH were measured by chemical luminescence immunity assay. The results demonstrated that no significant difference was observed in serum FSH levels and expression levels of placental FSH mRNA and protein between normal pregnancy and pre‑eclampsia. However, RT‑qPCR results indicated that the expression level of FSHR mRNA in pre‑eclamptic placental samples was significantly lower than normal pregnancies. Immunostaining results from normal pregnant samples indicated that the FSHR protein was strongly expressed in the endothelial cells of blood vessels in the chorionic villi, moderately expressed in stromal cells of the villus, but not expressed in trophoblast cells of the term placenta. The staining intensity of FSHR‑positive area was significantly lower in the placental villi of pre‑eclampsia, when compared with the normal control group. In conclusion, expression levels of placental FSHR mRNA and protein are significantly reduced in pregnancies complicated with pre‑eclampsia in the present study. Further studies may investigate whether FSHR could be used as a biomarker for the prediction of pre‑eclampsia.

The antioxidant potential of Actinidia macrosperma C. F. Liang (Actinidiaceae) was investigated in vitro for total phenolic content, along with total antioxidant activity (TAA), 1,1-diphenyl 2-picryl hydrazyl (DPPH), and lipid peroxidation (LP). The results indicated that different polarity extracts of A. macrosperma exhibit different biological activities, which depends mainly on the presence of phenolic compounds. The antioxidant activity was in the following decreasing order: MeOH extract > EtOAc extract > aqueous extract > CHCl3 extract > Hexane extract. Moreover, the cytotoxic activity of this plant by MTT dye assay using SMMC-7721 has been determined also. The hexane, EtOAc, and CHCl3 extracts showed cytotoxicity in a dose-dependent manner. Methanol and aqueous extracts, however, showed weak activities in this test. And a very significant cytotoxic activity, not significantly different from the positive control of quercetin, was observed in CHCl3 extract.