Mitochondria-targeted antioxidant mitoquinone mitigates vitrification-induced damage in mouse ovarian tissue by maintaining mitochondrial homeostasis via the p38 MAPK pathway

作者：Tianqi Du, Han Su, Dan Cao, Qingxia Meng, Ming Zhang, Zhenxing Liu, Hong Li · 发表于：European journal of medical research · 年份：2024 · DOI：10.1186/s40001-024-02181-z · 被引用次数：9 · 研究领域：Reproductive Biology and Fertility、Mitochondrial Function and Pathology、Coenzyme Q10 studies and effects

OBJECTIVE: Ovarian tissue cryopreservation has become a promising alternative for fertility preservation in cancer patients, allowing ovarian tissue to be stored for future autotransplantation. Oxidative stress damage occurring during the cryopreservation process may impact tissue quality and function. This study aims to investigate the protective effects and potential mechanisms of Mitoquinone (MitoQ), a mitochondria-targeted derivative of the antioxidant ubiquinone, during the vitrification of ovarian tissue in mice. METHODS: KGN cells were treated with various concentrations (0.1, 1, 10, and 50 μM) of MitoQ to determine the optimal concentration. Female ICR mice were divided into three groups: control, conventional vitrification, and MitoQ-supplemented vitrification. Ovarian samples were cryopreserved, thawed, and assessed for tissue morphology using Hematoxylin and Eosin (H&E) staining, and mitochondrial changes using immunofluorescence, transmission electron microscopy, and Western blot analysis. RNA sequencing (RNA-seq) was employed to explore potential protective mechanisms. Autotransplantation experiments were conducted, and the long-term effects of MitoQ on ovarian function were evaluated by counting follicle numbers through H&E staining and measuring serum estradiol and AMH levels using ELISA. RESULTS: MitoQ at 1 μM was found to be the optimal concentration for maintaining follicular morphology after vitrification. It effectively reduced mitochondrial oxidative dama...