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Melatonin improves the structure and function of autografted mice ovaries through reducing inflammation: A
Maryam Noori Hassanvand1, Malek Soleimani Mehranjani1, Elham Shojafar1
1Department of Biology, Faculty of Science, Arak University, Arak 381-5688138, Iran.
Abstract:
Melatonin has anti-oxidant, anti-inflammatory and anti-apoptotic properties. We aimed to investigate the effect of melatonin on the structure and function of mice ovaries following autograft transplantation. NMRI mice were divided into: control, autografted + saline, autografted + melatonin (20 mg/kg/day i.p. injection for 1 day before until 7 days after transplantation). 28 days post transplantation, ovary compartments were studied stereologically. Follicle apoptosis and the level of progesterone and estradiol were also measured. The inflammation, serum MDA concentration and total antioxidant capacity were also assessed on day 7 post transplantation. The total volume of the ovary, cortex and medulla (P < 0.05) and the number of different types of follicles (P < 0.001), the concentration of IL-10, progesterone and estradiol (P < 0.001) and TAC (P < 0.01) significantly decreased in the autografted + saline group compared to the control. The levels of IL-6 (P < 0.01), TNF-α, MDA and the apoptotic rate (P < 0.001) increased significantly in the autografted + saline group compared to the control, while the total volume of the ovary, cortex and medulla (P < 0.05) and the number of different types of follicles (P < 0.001), the concentration of IL-10, progesterone and estradiol (P < 0.001) and TAC (P < 0.01) significantly increased in the autografted + melatonin group compared to the autografted + saline group. The levels of IL-6 (P < 0.01), TNF-α, MDA and the apoptotic rate (P < 0.001) decreased significantly in the autografted + melatonine group compared to the autografted + saline group. In the autografted + melatonin group, the localization of CD31-positive cells in the theca layer was similar to the control group. Melatonin can improve the structure and function of the grafted ovary.
Insights
Melatonin treatment improved the structure and function of grafted mouse ovaries. It reduced apoptosis and inflammation while enhancing ovarian volume and follicle count.
Area of Science:
- Reproductive Biology
- Endocrinology
- Transplantation Science
Background:
- Ovarian autograft transplantation is crucial for fertility preservation.
- Grafted ovaries face challenges like oxidative stress, inflammation, and apoptosis.
- Melatonin is known for its antioxidant, anti-inflammatory, and anti-apoptotic properties.
Purpose of the Study:
- To investigate the protective effects of melatonin on mouse ovarian structure and function after autograft transplantation.
- To evaluate melatonin's impact on ovarian tissue integrity, follicle survival, and hormonal balance.
Main Methods:
- NMRI mice underwent ovarian autograft transplantation.
- Groups included control, autografted + saline, and autografted + melatonin (20 mg/kg/day).
- Ovarian structure, follicle apoptosis, hormone levels (progesterone, estradiol), inflammation markers (IL-6, TNF-α), oxidative stress (MDA), and total antioxidant capacity (TAC) were assessed.
Main Results:
- Autografted ovaries treated with saline showed decreased ovarian volume, follicle count, progesterone, estradiol, and TAC, alongside increased IL-6, TNF-α, MDA, and apoptosis.
- Melatonin treatment significantly improved ovarian volume, follicle count, progesterone, estradiol, and TAC compared to the saline group.
- Melatonin also significantly reduced IL-6, TNF-α, MDA, and apoptosis rates in grafted ovaries.
Conclusions:
- Melatonin administration effectively mitigates the detrimental effects of oxidative stress and inflammation following ovarian autograft transplantation.
- Melatonin treatment preserves ovarian structure and function, making it a promising therapeutic agent for improving outcomes in ovarian transplantation.
- The observed improvements suggest melatonin's potential to enhance the viability and success rate of ovarian autografts.
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