Yang Juan, Xu Rui, Luan Yingying, Fan Hancheng, Yang Shuo, Liu Jun, Zeng Huihong, Shao Lijian
School of Public Health, Jiangxi Provincial Key Laboratory of Preventive Medicine, Nanchang University, Nanchang, China.
Department of Blood Transfusion, Affiliated Hospital of Chengde Medical College, Chengde, China.
Front Cell Dev Biol. 2022 Apr 25;10:783884. doi: 10.3389/fcell.2022.783884. eCollection 2022.
Male infertility is an important problem in human and animal reproduction. The testis is the core of male reproduction, which is very sensitive to radiation. The decline of male reproductive ability is a common trend in the world. Radiation is a physical factor leading to abnormal male reproductive function. To investigate the potential mechanisms of testicular damage induced by radiation and explore effective strategies to alleviate radiation-induced testis injury, C57BL/6 mice were irradiated with 8.0 Gy of X-ray irradiation. Testis and epididymis were collected at days 1, 3, and 7 after radiation exposure to analyze spermatogonia and sperm function. The results showed that radiation significantly destroyed testicular structure and reduced the numbers of spermatogonia. These were associated with mTORC1 signaling activation, decreased cellular proliferation and increased apoptotic cells in the irradiated testis. Rapamycin significantly blocked mTORC1 signaling pathway in the irradiated testis. Inhibition of mTORC1 signaling pathway by rapamycin treatment after radiation could significantly improve cell proliferation in testis and alleviate radiation-induced testicular injury after radiation exposure. Rapamycin treatment benefited cell survival in testis to maintain spermatogenesis cycle at 35 days after irradiation. These findings imply that rapamycin treatment can accelerate testis recovery under radiation condition through inhibiting mTORC1 signaling pathway.
男性不育是人类和动物生殖中的一个重要问题。睾丸是男性生殖的核心,对辐射非常敏感。男性生殖能力下降是全球的一个普遍趋势。辐射是导致男性生殖功能异常的一个物理因素。为了研究辐射诱导睾丸损伤的潜在机制,并探索减轻辐射诱导睾丸损伤的有效策略,对C57BL/6小鼠进行8.0 Gy的X射线照射。在辐射暴露后的第1、3和7天收集睾丸和附睾,以分析精原细胞和精子功能。结果表明,辐射显著破坏了睾丸结构,减少了精原细胞数量。这些与mTORC1信号激活、照射睾丸中细胞增殖减少和凋亡细胞增加有关。雷帕霉素显著阻断了照射睾丸中的mTORC1信号通路。辐射后用雷帕霉素处理抑制mTORC1信号通路可显著改善睾丸中的细胞增殖,并减轻辐射暴露后辐射诱导的睾丸损伤。雷帕霉素处理有利于照射后35天睾丸中的细胞存活,以维持精子发生周期。这些发现表明,雷帕霉素处理可通过抑制mTORC1信号通路在辐射条件下加速睾丸恢复。