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首页> 外文期刊>Toxicology Letters: An International Journal Providing a Forum for Original and Pertinent Contributions in Toxicology Research >4-Nonylphenol induces autophagy and attenuates mTORp70S6K/4EBP1 signaling by modulating AMPK activation in Sertoli cells
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4-Nonylphenol induces autophagy and attenuates mTORp70S6K/4EBP1 signaling by modulating AMPK activation in Sertoli cells

机译：4-壬基酚诱导自噬并通过调节Sertoli细胞中的AMPK活化来诱导MTORP70S6K / 4EBP1信号传导

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The estrogenic chemical 4-nonylphenol (NP) is known to impair testicular devolopment and spermatogenesis in rodents. The objective of this study was to explore the effects of NP on autophagy induction and AMPK-mTOR signaling pathway in Sertoli cells (SCs), which are the "nursemaid cells" for meiosis of spermatocytes. In this study we exposed 7-week-old male rats to NP by intra-peritoneal injection at 0, 20, 50 or 100 mg/kg body weight/2 days for 20 consecutive days. Our results showed that exposure to NP dose-dependently induces the formation of autophagosomes in SCs, increases the expression of Beclin-1, the conversion of LC3-I to LC3-II and the mRNA expression of Atg3, Atg5, Atg7 and Atg12 in testis, and these effects are concomitant with the activation of AMPK, and the suppression of TSC2-mTOR-p70S6K/4EBP1 signaling cascade in testis. Furthermore, 10 mu M Compound C or AMPI kappa alpha l siRNA pre-treatment effectively attenuated autophagy and reversed AMPK-mTOR-p70S6K/4EBP1 signaling in NP-treated SCs. Co-treatment with 1 mM AICAR remarkably strengthened NP-induced autophagy and mTOR inhibition in SCs. Together, these data suggest that NP stimulates Sertoli cell autophagy and inhibits mTOR-p70S6KRIEBP1 activity through AMPK activation, which is the potential mechanism responsible for the regulation of testis function and differentiation following NP exposure. (C) 2016 Elsevier Ireland Ltd. All rights reserved.
机译：已知雌激素化学4-壬基酚（NP）损害啮齿动物中的睾丸促血散和精子发生。本研究的目的是探讨NP对Sertoli细胞（SCS）中的自噬诱导和AMPK-MTOR信号传导途径的影响，这是精子细胞的减数分裂的“保育群细胞”。在这项研究中，我们通过腹膜内注射在0,20,50或100mg / kg体重/ 2天连续20天暴露7周龄雄性大鼠NP。我们的结果表明，暴露于NP剂量依赖性诱导SCS中自噬体的形成，增加了BECLIN-1的表达，LC3-I至LC3-II的转化率和ATG3，ATG5，ATG7和ATG12中的mRNA表达在睾丸中，这些效果伴随着AMPK的激活，以及睾丸中的TSC2-MTOR-P70S6K / 4EBP1信号传导级联的抑制。此外，10μM化合物C或AMPI Kappaα1siRNA预处理有效地衰减了NP处理的SCS中的自噬和逆转AMPK-MTOR-P70S6K / 4EBP1信号传导。用1mm AICAR共同治疗显着强化SCS中的NP诱导的自噬和MTOR抑制。这些数据表明，NP通过AMPK激活刺激Sertoli细胞自噬并抑制MTOR-P70S6KRIEBP1活性，这是对NP暴露后调节睾丸功能和分化负责的潜在机制。 （c）2016 Elsevier Ireland Ltd.保留所有权利。

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