Abstract: Objective To investigate the therapeutic effect of transplantation of menstrual stem cells (MenSCs) on rat model of polycystic ovary syndrome (PCOS). Methods A total of 45 female SD rats were divided into 3 groups. The control group was not treated. The PCOS group was intramuscularly injected with dehydroepiandrosterone (DHEA, 60 mg/ kg) to induce PCOS. The transplant group was intramuscularly injected with DHEA. After 3 weeks, the MenSCs suspension was injected through the tail vein. After 5 weeks of feeding, venous blood was taken. ELISA kit was used to detect folliclestimulating hormone (FSH), luteinising hormone (LH), estradiol (E2), progesterone (P), testosterone (T) and prolactinemia(PRL) levels. Ovarian tissues were taken for HE staining to observe ovarian morphology. qPCR was used to detect miRNA-135 expression in ovarian tissue. Western blot assay was used to detect the expression of Bax and Bcl-2 proteins in ovarian tissue. Results The FSH level was significantly decreased, and LH and T levels were significantly increased, in the PCOS group than those in the control group (P＜0.05). The FSH level was significantly increased, and LH and T levels were significantly decreased in the transplantation group than those in the PCOS group (P＜0.05). The follicle morphology was normal in the control group. Follicles with more cystic dilatation in ovary were observed in the PCOS group. The follicles with polycystic expansion were less in the transplantation group than those in the PCOS group. The expressions of miRNA-135 and Bcl-2 protein were significantly decreased in the PCOS group than those in the control group, and the expression of Bcl-2 protein was significantly higher in the PCOS group than that in the control group (P＜0.05). The expressions of miRNA-135 and Bcl-2 protein were significantly higher, the expression of Bas was significantly decreased, in the transplantation group than those of PCOS group (P＜0.05). Conclusion MenSCs has a significant improvement effect on rat PCOS, which may be achieved by up-regulating the expression of miRNA-135 and then regulating the Bax/Bcl-2 pathway.

Key words: polycystic ovary syndrome, disease models, animal, stem cell transplantation, miRNA-135, Bax, Bcl-2