Rapamycin Ameliorates Radiation-Induced Testis Damage in Mice.
Rapamycin Ameliorates Radiation-Induced Testis Damage in Mice.
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雷帕霉素可改善辐射引起的小鼠睾丸损伤
DOI：
10.3389/fcell.2022.783884
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发表时间：
2022
影响因子：
5.5
通讯作者：
中科院分区：
文献类型：
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作者：
雄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世界范围内的普遍趋势。辐射是导致男性生殖功能异常的物理因素。为探讨放射性睾丸损伤的可能机制，探讨减轻放射性睾丸损伤的有效策略，采用8.0戈伊X线照射C57 BL/6小鼠。分别于照射后第1、3、7天取睾丸和附睾，分析精原细胞和精子功能。结果表明，辐射可明显破坏睾丸结构，减少精原细胞数量。这些都与mTORC 1信号激活，减少细胞增殖和增加辐射睾丸中的凋亡细胞。雷帕霉素显著阻断照射睾丸中mTORC 1信号通路。雷帕霉素抑制辐射后mTORC 1信号通路可显著促进睾丸细胞增殖，减轻辐射后睾丸损伤。照射后35天，雷帕霉素处理有利于睾丸细胞存活，维持精子发生周期。这些结果表明，雷帕霉素处理可以通过抑制mTORC 1信号通路促进辐射条件下睾丸的恢复。
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.
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影响因子：
64.5
作者：
Hobbs RM;Seandel M;Falciatori I;Rafii S;Pandolfi PP
通讯作者：
Pandolfi PP
影响因子：
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作者：
Aboul Fotouh GI;Abdel-Dayem MM;Ismail DI;Mohamed HH
通讯作者：
Mohamed HH
影响因子：
3.3
作者：
Klopp, Ann;Smith, Benjamin D;Alektiar, Kaled;Cabrera, Alvin;Damato, Antonio L;Erickson, Beth;Fleming, Gini;Gaffney, David;Greven, Kathryn;Lu, Karen;Miller, David;Moore, David;Petereit, Daniel;Schefter, Tracey;Small, William Jr;Yashar, Catheryn;Viswanathan, Akila N
通讯作者：
Viswanathan, Akila N
影响因子：
28.5
作者：
Oermann EK;Suy S;Hanscom HN;Kim JS;Lei S;Yu X;Zhang G;Ennis B;Rohan JP;Piel N;Sherer BA;Borum D;Chen VJ;Batipps GP;Constantinople NL;Dejter SW;Bandi G;Pahira J;McGeagh KG;Adams-Campbell L;Jha R;Dawson NA;Collins BT;Dritschilo A;Lynch JH;Collins SP
通讯作者：
Collins SP
影响因子：
5.8
作者：
Citrin, Deborah;Cotrim, Ana P.;Mitchell, James B.
通讯作者：
Mitchell, James B.