Background: Endometrial regeneration is essential for normal endometrial function; however, it is unclear whether and how menstrual blood-derived stem cells (MenSCs) and platelet-derived growth factor (PGDF) are associated with this phenomenon. The present study explored this topic. Material/Methods: EM-E6/E7/hTERT cells were divided into 5 groups: control group, NC group, PDGF group, MenSCs group, and PDGF+MenSCs group. The effects of MenSCs and PDGF on cell proliferation, invasion, and microvascular formation of endometrial epithelium were investigated by CCK-8, Transwell, and tube formation assays, respectively. Mouse endometrial injury models were established and mice were randomly divided into control, model, PDGF, MenSCs, and PDGF+MenSCs groups. Pathological change was examined with hematoxylin and eosin (H&E) staining. Microvessel formation of endometrial epithelium was estimated by detecting the expression of CD34 protein with immunohistochemical (IHC) staining. Western blot analysis was used to detect the activation of Akt and Bad proteins in endometrial tissue. Results: MenSCs, PDGF, and the combination treatments significantly promoted the proliferation, migration, and tube formation of endometrial epithelium compared to the control and NC group. The combination of MenSCs and PDGF remarkably promoted re-epithelialization and endometrial repair. IHC staining analysis showed significant increases in CD34 expression of the endometrial tissue following treatment with PDGF and MenSCs. The combination treatments also markedly enhanced the phosphorylation of Akt and Bad in endometrial tissue. Conclusions: These results suggest that MenSCs and PDGF may be candidate substances for endometrial injury repair.

MicroRNAs (miRNAs), which is a type of non-coding and single-stranded small molecule RNA, bind either completely or incompletely to 3'-UTR of the target gene mRNA to inhibit mRNA translation or degradation. In our study, we aimed to explore the roles and mechanisms of miR-181c in the apoptosis of RL95-2 human endometrial carcinoma cells. Cell activity and apoptosis were detected by cell counting Kit-8 (CCK-8) assay and flow cytometry (FCM), respectively. Related mRNAs and proteins expression was determined by quantitative real-time reverse transcription PCR (qRT-PCR) and western blot assays, respectively. The binding capacity of PTEN-3'-UTR and miR-181c was assessed by luciferase reporter assay. The obtained results suggested that E2 evidently increased the cell activity of RL95-2 cells. In addition, miR-181c inhibitor suppressed the cell viability and enhanced the apoptosis capacity of E2-induced RL95-2 cells and distinctly reduced the miR-181c expression. We also found that miR-181c could bind to PTEN-3'-UTR and miR-181c inhibitor up-regulated the expression level of PTEN in E2-induced RL95-2 cells. Besides, overexpression of PTEN markedly promoted the apoptosis of E2-induced RL95-2 cells through regulating the Bax and Bcl-2 expression, and modulated the expression of AKT pathway, p53 and Cyclin D. In conclusion, our findings revealed that miR-181c affected the estrogen-dependent endometrial carcinoma cell growth by targeting PTEN. The potential effects of miR-181c on the apoptosis of E2-induced RL95-2 cells suggest that miR-181c could be an effective target for endometrial carcinoma therapies.

Background: We aimed to explore the clinical efficacy of vitamin D combined with metformin and clomiphene in the treatment of patients with polycystic ovary syndrome combined with infertility. Methods: Overall, 396 cases of polycystic ovarian syndrome combined with infertility in Yantai Yuhuangding Hospital, Yantai, China were prospectively analyzed. Among them, 204 cases treated with vitamin D combined with metformin and clomiphene were set as the study group; 192 cases treated with only metformin and clomiphene were set as the control group. The ovarian volume and thickness of uterine wall before and after treatment were recorded. Levels of fasting insulin (FINS), luteinizing hormone (LH), testosterone (T), folliclestimulating hormone (FSH), and estradiol (E2) before and after treatment were recorded. Results: There was no difference in body weight, BMI, ovarian volume, thickness of ovarian wall, FINS, LH, T, FSH and E2 between the study group and the control group; there was no significant difference in FSH, E2 and the thickness of uterine wall between the two groups. After treatment, the BMI, FINS, LH, and T in the study group were significantly lower than those in the control group (P<0.05); the incidence rates of oligomenorrhea, facial acne and hairy symptoms in the study group were significantly lower than those in the control group (P<0.05); after treatment, the ovulation rate and pregnancy rate in 36 cycles in the observation group were significantly higher than those of the control group (P<0.05). Conclusion: Our challenge could significantly improve clinical symptoms and endocrine conditions, and greatly enhance the ovulation rate and pregnancy rate.