Rosuvastatin mitigates ovarian ischemia-reperfusion injury in rats by modulating oxidative stress, inflammation, and angiogenesis.

Objective

To investigate the protective effects of rosuvastatin against ovarian ischemia-reperfusion injury (I/R) in a rat model.

Design

Controlled experimental study using an induced ovarian torsion-detorsion model. SUBJECTS Fifty adults female Wistar rats (aged 8-10 weeks, weighing 100-150 g). EXPOSURE Intraperitoneal administration of rosuvastatin (5 mg/kg) 30 minutes before induction of ischemia in the designated treatment groups. MAIN OUTCOME MEASURES Ovarian tissue levels of myeloperoxidase (MPO), malondialdehyde (MDA), total antioxidant capacity (TAC), and activities of superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT); mRNA expression of vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), tumor necrosis factor-α (TNF-α), and caspase-3; and semi-quantitative histopathological scoring of tissue damage.

Results

Ischemia and I/R significantly elevated MPO, MDA, VEGF, bFGF, TNF-α, and caspase-3 levels while worsening histological damage. Rosuvastatin pretreatment reduced MPO by 13%-16%, MDA by 9%, VEGF by 7%-14%, bFGF by 14%-37%, TNF-α by 34%-38%, and caspase-3 by 31%-39%; increased TAC by 20%; and markedly improved histopathological scores, including reduced follicular atresia. No significant changes were observed in SOD, GPx, or CAT activities.

Conclusions

Rosuvastatin exerts protective effects against ovarian I/R by attenuating oxidative stress, inflammation, excessive angiogenesis, and apoptosis, independent of major antioxidant enzyme induction. These preclinical findings suggest potential adjunctive utility in limiting reperfusion injury after detorsion; however, protein-level validation, dose-response studies, post-ischemic administration, long-term fertility outcomes, and safety assessments are required before any clinical translation.