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自噬参与热暴露小鼠睾丸中Nrf2抗氧化系统的激活。

Autophagy involved in the activation of the Nrf2-antioxidant system in testes of heat-exposed mice.

作者信息

Li Zhaojian, Li Yansen, Zhou Xin, Dai Pengyuan, Li Chunmei

机构信息

College of Animal Science and Technology, Nanjing Agricultural University, Nanjing 210095, China.

College of Animal Science and Technology, Nanjing Agricultural University, Nanjing 210095, China.

出版信息

J Therm Biol. 2018 Jan;71:142-152. doi: 10.1016/j.jtherbio.2017.11.006. Epub 2017 Nov 13.

Abstract

Hyperthermia causes oxidative stress in testes, which triggers antioxidant signals including autophagy and nuclear factor erythroid 2-related factor 2 (Nrf2). However, their relationship in testes under oxidative stress is unclear. In this study, we conducted testes injection for autophagy alteration and heat exposure to reveal the interaction between autophagy and the Nrf2-antioxidant system. Male mice were injected once with normal saline as control (Cont group), autophagy inhibitor 3-methyladenine (3-MA group) or autophagy inducer rapamycin (Rapa group). Then, each group was divided into two parts: one received a 2-h 42°C heat treatment for eight days (HT groups), and the other was kept thermal neutral (NT groups). Heat-exposed mice showed significantly increased rectal, scrotal surface and body surface temperatures. Histology of the testes revealed many vacuoles inserted in the seminiferous tubules in the HT Cont group and two 3-MA groups. Ultrastructural changes in germ cells revealed autophagosomes in two 3-MA groups. Immunohistochemical detection of Nrf2 and p62/SQSTM1 proteins showed prominent expression in Leydig cells. Heat exposure increased Nrf2 protein and mRNA levels. 3-MA and Rapa testes injection also resulted in Nrf2 cytoplasm accumulation. Massive conversion of LC3 (microtubule-associated protein light chain 3)Ⅰ to LC3Ⅱ was detected in two 3-MA groups, accompanied by decreased ATG5 (autophagy related gene 5) mRNA levels in the HT 3-MA group. These results indicated autophagy alteration triggered the Nrf2 signaling pathway with consequences such that the autophagy inducer protected the testes and the autophagy inhibitor enhanced the detrimental effects caused by heat exposure.

摘要

高温会导致睾丸产生氧化应激,进而触发包括自噬和核因子红细胞2相关因子2(Nrf2)在内的抗氧化信号。然而,在氧化应激状态下它们在睾丸中的关系尚不清楚。在本研究中,我们通过睾丸注射来改变自噬并进行热暴露,以揭示自噬与Nrf2-抗氧化系统之间的相互作用。雄性小鼠一次性注射生理盐水作为对照(Cont组)、自噬抑制剂3-甲基腺嘌呤(3-MA组)或自噬诱导剂雷帕霉素(Rapa组)。然后,每组分为两部分:一部分接受为期八天的2小时42°C热处理(HT组),另一部分保持热中性(NT组)。热暴露小鼠的直肠、阴囊表面和体表温度显著升高。睾丸组织学检查显示,HT Cont组和两个3-MA组的生精小管中有许多空泡。生殖细胞的超微结构变化显示两个3-MA组中有自噬体。Nrf2和p62/SQSTM1蛋白的免疫组化检测显示在睾丸间质细胞中有显著表达。热暴露增加了Nrf2蛋白和mRNA水平。3-MA和Rapa睾丸注射也导致Nrf2在细胞质中积累。在两个3-MA组中检测到微管相关蛋白轻链3(LC3)Ⅰ大量转化为LC3Ⅱ,同时HT 3-MA组中自噬相关基因5(ATG5)的mRNA水平降低。这些结果表明自噬改变触发了Nrf2信号通路,其结果是自噬诱导剂保护了睾丸,而自噬抑制剂增强了热暴露所造成的有害影响。

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