卵泡发生
辅酶Q10
增殖细胞核抗原
生物
抗苗勒氏激素
促卵泡激素受体
卵巢
男科
内分泌学
内科学
卵巢早衰
活性氧
卵巢储备
促卵泡激素
胚胎
激素
免疫学
医学
免疫组织化学
胚胎发生
细胞生物学
不育
促黄体激素
遗传学
怀孕
作者
Aref Delkhosh,Masoud Delashoub,Ali Asghar Tehrani,Ali Mohammad Bahrami,Vahid Niazi,Hamed Shoorei,Majid Banimohammad,Hossein Kalarestaghi,Majid Shokoohi,Amin Agabalazadeh,Mahdi Mohaqiq
摘要
Abstract Cyclophosphamide (CTX) has been broadly used in the clinic for the treatment of autoimmune disorders and ovarian cancer. The process of chemotherapy has significant toxicity in the reproductive system as it has detrimental effects on folliculogenesis, which leads to an irreversible premature ovarian failure (POF). Coenzyme Q10 (CoQ10) has positive impacts on the reproductive system due to its antioxidant properties, protecting the cells from free‐radical oxidative damage and apoptosis. However, little is known about the possible synergistic effect of CTX and CoQ10 on the expression of genes involved in folliculogenesis, such as proliferation cell nuclear antigen (PCNA) and follicle‐stimulating hormone receptor (FSHR). A total of 32 NMRI mice were applied and divided into four groups, including healthy control, CTX, CTX + CoQ10, and CoQ10 groups. The effects of CoQ10 on CTX‐induced ovarian injury and folliculogenesis were examined by histopathological and real‐time quantitative reverse transcription‐polymerase chain reaction analyses. The rates of fertilization (in vitro fertilization), embryo development, as well as the level of reactive oxygen species (ROS) in metaphase II (MII) mouse oocytes after PMSG/HCC treatment were also assessed. Results showed that the treatment with CTX decreased the mRNA expression of PCNA and FSHR, IVF rate, and embryo development whereas the application of CoQ10 successfully reversed those factors. CoQ10 administration significantly enhanced histological morphology and decreased ROS levels and the number of atretic follicles in the ovary of CTX‐treated mice. In conclusion, it seems that the protective effect of CoQ10 is exerted via the antioxidant and proliferative properties of this substance on CTX‐induced ovarian damage.
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