Effects of Mesenchymal Stem Cell Transplantation on the Bcl-2 mRNA, p21 mRNA, and survivin mRNA Expression in Endometriosis Model Mice
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preprint
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AI-generated summary
Mesenchymal stem cell transplantation in endometriosis model mice did not significantly alter Bcl-2, p21, or survivin mRNA expression, suggesting no effect on granulosa cell apoptosis.
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Abstract
Background. In endometriosis, there is an increase in ROS levels and can cause a damage the DNA structures. Objectives. To analyze the effect of mesenchymal stem cells on the expression of BCl2 mRNA, p21 mRNA, and Survivin mRNA in mice with endometriosis models. Material and methods. This study used 42 female mice which were divided into 3 groups, the normal mice group (T0), the positive control group, the endometriosis model group that received placebo (T1) and the endometriosis model mice that received bone marrow mesenchymal stem cells (T2). The stages of this research are: endometrial biopsy, bone marrow isolation for mesenchymal stem cell production, mesenchymal stem cell production, endometriosis model making, mesenchymal stem cell therapy in endometriosis model mice, cumulus-oocyte complex (COC) sample collection. Real-time PCR and Examination of Bcl-2 mRNA expression, p21 mRNA expression, and survivin mRNA expression, using real-time PCR method. Data analysis using ANOVA. Results. There was PKH26 luminescence as a characteristic sign of homing mesenchymal stem cells in the ovaries of mice that received mesenchymal stem cells. The values of Bcl-2 mRNA, p21 mRNA, and survivin mRNA of the three groups were not significantly different (p> 0.05), although the mean Bcl-2 mRNA expression in the endometriosis model group given mesenchymal stem cells was higher than the endometriosis model group. Conclusions. There was no effect between the expression of Bcl-2 mRNA, p21 mRNA, and survivin mRNA on the decrease in apoptosis of granulosa cells in the group of endometriosis model mice that received mesenchymal stem cells.
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Source provenance
- europepmc
- last seen: 2026-10-18T09:30:06.152893+00:00
- openalex
- last seen: 2026-06-10T17:14:06.276822+00:00
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