Introduction. Freezing of ovarian tissue is used for preservation of fertility. The freezing-thawing process is accompanied by oxidative stress and induction of apoptosis. Apoptosis is a complex process that has been studied in animal models. The present study was aimed at investigating the effect of selenium on suppression of apoptosis during vitrification-thawing process of mice ovary via studying expression of apoptosis-related genes, and also, we aimed to design statistical models for the roles of single genes and gene-gene interactions in suppression of apoptosis. Methods. A total of 10 right ovary samples from 10 mice were randomly divided into two groups of selenium treatment (at dose 5 μg/ml sodium selenite, through adding to the media) and control group. Vitrification-thawing process was done according to the existed protocols. Real-time PCR was used for gene expression study. The apoptosis gene profile included P53, Bax, Fas, and Bcl-2. General linear model was applied to study single gene associations and gene-gene interactions. Results. From the studied genes, P53 showed a significant downregulation in the selenium group in comparison to the control group (∆∆CT=1.96; P=0.013; relative expression RE=0.28). Bcl-2 showed a significant upregulation in the selenium group in comparison to the control group (∆∆CT=−2.49; P<0.001; RE=3.49). No significant result was found for other genes. According to the multiple models, Bcl-2 showed a protective single gene association (beta=−0.33; P=0.032), and Fas∗Bcl-2 interaction was significantly positive (beta=0.19; P=0.036). Conclusion. Addition of selenium to cryomedia of vitrification-thawing process could reduce the apoptosis induced by freezing-thawing stress in mice ovary via downregulation of P53 and upregulation of Bcl-2 at transcription level. Multivariable statistical models should be performed in future researches to study biological systems.

Objective: Progesterone (P4) is known to directly affect ovarian tissue angiogenesis. The present study was designed to show how P4 affects ovarian angiogenesis in hormonal, histological, and molecular levels. Methods: Fifteen adult female NMRI mice were divided into three groups: Control Group; Case Group I (ovarian stimulation alone); and Case Group II (ovarian stimulation followed by P4 administration). Blood and ovarian tissue samples were assessed for hormonal, histological, and molecular alterations. Gene expression for ovarian vascular endothelium growth factor (VEGF) and hypoxia-inducible factor-1 alpha (HIF-1α) was analyzed using real-time PCR. Results: Ovarian hormone levels were increased in the case groups compared with the control group ( p <0.05). Quantitative corpus luteum parameters were increased in the case groups compared with the control group ( p <0.05). Quantitative ovarian vascular parameters were significantly different in the case groups compared with the control group. Gene expression analyses shows that the mice in Case Group I had higher levels of ovarian VEGF expression than the mice in the control group ( p <0.05). No significant difference in gene expression was observed for HIF-1ɑ. Conclusion: Treatment with P4 after ovarian stimulation enhanced ovarian angiogenesis by increasing hormone levels and causing significant structural changes.

Objective Mast cell population and histamine affect on blastocyst implantation. This study aimed to evaluate the effects of progesterone administration after induction of ovulation on the uterine tissue mast cell population and histamine content in mice. Methods We ran an experimental study on three groups of mice; control group, ovulation induction (induction group), and ovulation induction along with progesterone administration (progesterone group). Mast cells were counted using toluidine blue staining, and the histamine level was measured through spectrophotometry. Results According to the analysis of variance (ANOVA), there was no difference in mast cell population in endometrium ( p =0.138) nor in myometrium ( p =0.611). The ratio of mast cells in the myometrium per endometrium increased in the progesterone group in comparison to the control group based on a generalized linear model ( p =0.041). The uterine histamine level was different between the groups, based on the ANOVA ( p =0.039), in which the progesterone group had lower amounts of histamine. Conclusions Progesterone administration after ovulation induction did not decrease the number of endometrial mast cells and could have increased the ratio of myometrium mast cells per endometrium mast cell. The histamine level in uterus decreased by the administration of progesterone in the ovulation-induced mice.