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Protective Role of Spermidine Against Diabetes-Induced Ovarian and Endometrial Injury via LC3 and Beclin-1 Modulation
Bakiye Akbaş1, Gülseren Dinç1, Ahmet Akbaş2
1Department of Obstetrics and Gynecology, Medical Faculty, Karadeniz Technical University, Trabzon 61080, Turkey.
Abstract:
Background: Diabetes mellitus adversely affects female reproductive health by inducing oxidative stress, impairing autophagy, and promoting fibrotic remodeling in ovarian and uterine tissues. Spermidine, a natural polyamine, has gained attention as an antioxidant and autophagy enhancer. This study aimed to investigate the potential protective role of spermidine against diabetes-induced reproductive injury in rats. Methods: Thirty adult female Wistar rats were randomly divided into three groups (n = 10 each): Control, Diabetes, and Diabetes + Spermidine. Diabetes was induced with streptozotocin (60 mg/kg, i.p.). After confirmation of hyperglycemia (≥250 mg/dL), rats received either saline or spermidine (40 mg/kg/day, oral gavage) for four weeks. At sacrifice, plasma anti-Müllerian hormone (AMH) levels were determined, and ovarian and uterine tissues were assessed histologically and biochemically for oxidative stress markers (GSH, MDA, Nrf2), autophagy proteins (LC3, Beclin-1), and fibrosis indicators (TGF-β, histological scoring). Results: Diabetic rats exhibited severe hyperglycemia, pronounced follicular and endometrial degeneration, increased fibrosis, reduced plasma AMH, depleted GSH, SOD, CAT, GPx and Nrf2, and elevated MDA (p < 0.001). Spermidine treatment significantly mitigated these alterations, lowering glucose levels, alleviating histopathological injury, elevating the antioxidant defense (GSH, SOD, CAT, GPx) and the Nrf2 and decreasing MDA and TGF-β concentrations (p < 0.05 vs. Diabetes). Moreover, spermidine supplementation enhanced LC3 and Beclin-1 expression, suggesting improved autophagic activity. Conclusions: Spermidine counteracts diabetes-induced ovarian and uterine damage by reinforcing antioxidant defense, stimulating autophagy, and limiting fibrosis. These findings highlight spermidine as a promising adjunctive agent to support female reproductive health under diabetic conditions.
Insights
Spermidine protects female rats from diabetes-induced reproductive damage by reducing oxidative stress, enhancing autophagy, and preventing fibrosis. This natural compound shows promise for improving reproductive health in diabetic conditions.
Area of Science:
- Reproductive Biology
- Endocrinology
- Toxicology
Background:
- Diabetes mellitus negatively impacts female reproductive health through oxidative stress, impaired autophagy, and fibrosis.
- Spermidine, a natural polyamine, is recognized for its antioxidant and autophagy-enhancing properties.
- This study investigates spermidine's protective effects against diabetes-induced reproductive injury in rats.
Purpose of the Study:
- To evaluate the efficacy of spermidine in mitigating diabetes-induced damage to ovarian and uterine tissues.
- To assess spermidine's impact on oxidative stress, autophagy, and fibrosis in the context of diabetes.
- To determine if spermidine can improve reproductive hormone levels in diabetic rats.
Main Methods:
- Thirty female Wistar rats were divided into Control, Diabetes, and Diabetes + Spermidine groups.
- Diabetes was induced using streptozotocin; spermidine (40 mg/kg/day) was administered orally for four weeks.
- Ovarian and uterine tissues were analyzed for oxidative stress markers, autophagy proteins, fibrosis indicators, and plasma anti-Müllerian hormone (AMH) levels.
Main Results:
- Diabetic rats showed hyperglycemia, tissue degeneration, increased fibrosis, reduced AMH, depleted antioxidants (GSH, SOD, CAT, GPx, Nrf2), and elevated MDA.
- Spermidine treatment significantly improved glucose levels, alleviated histopathological damage, and restored antioxidant defenses.
- Spermidine increased Nrf2, LC3, and Beclin-1 expression while decreasing MDA and TGF-β, indicating enhanced antioxidant activity, autophagy, and reduced fibrosis.
Conclusions:
- Spermidine effectively counteracts diabetes-induced ovarian and uterine damage in rats.
- The protective mechanisms involve reinforcing antioxidant defense, stimulating autophagy, and limiting fibrotic remodeling.
- Spermidine presents a potential therapeutic strategy for supporting female reproductive health in diabetic individuals.
