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首页> 美国卫生研究院文献>Toxins >The Effects of Autophagy and PI3K/AKT/m-TOR Signaling Pathway on the Cell-Cycle Arrest of Rats Primary Sertoli Cells Induced by Zearalenone
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The Effects of Autophagy and PI3K/AKT/m-TOR Signaling Pathway on the Cell-Cycle Arrest of Rats Primary Sertoli Cells Induced by Zearalenone

机译：自噬和PI3K / AKT / m-TOR信号通路对玉米赤霉烯酮诱导大鼠原代支持细胞的细胞周期阻滞的影响

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A high concentration of Zearalenone (ZEA) will perturb the differentiation of germ cells, and induce a death of germ cells, but the toxic mechanism and molecular mechanism remain unclear. The Sertoli cells (SCs) play an irreplaceable role in spermatogenesis. In order to explore the potential mechanism of ZEA male reproductive toxicity, we studied the effects of ZEA on cell proliferation, cell-cycle distribution, cell-cycle-related proteins and autophagy-related pathway the PI3K/Akt/mTOR signaling in primary cultured rats SCs, and the effects of autophagy and PI3K/AKT/m TOR signaling pathway on the SCs cell-cycle arrest induced by ZEA treated with the autophagy promoter RAPA, autophagy inhibitor CQ, and the PI3K inhibitor , respectively. The data revealed that ZEA could inhibit the proliferation of SCs by arresting the cell cycle in the G2/M phase and trigger the autophagy via inhibiting the PI3K/Akt/m TOR signaling pathway. Promoting or inhibiting the level of autophagy could either augment or reverse the arrest of cell cycle. And it was regulated by PI3K/Akt/m TOR signaling pathway. Taken together, this study provides evidence that autophagy and PI3K/Akt/m TOR signaling pathway are involved in regulating rats primary SCs cell-cycle arrest due to ZEA in vitro. To some extent, ZEA-induced autophagy plays a protective role in this process.
机译：高浓度的玉米赤霉烯酮（ZEA）将干扰生殖细胞的分化，并诱导生殖细胞死亡，但其毒性机理和分子机理尚不清楚。睾丸支持细胞（SCs）在精子发生中起着不可替代的作用。为了探索ZEA雄性生殖毒性的潜在机制，我们研究了ZEA对原代培养大鼠PI3K / Akt / mTOR信号传导，细胞周期分布，细胞周期相关蛋白和自噬相关途径的影响。 SCs，以及自噬和PI3K / AKT / m TOR信号通路对分别用自噬启动子RAPA，自噬抑制剂CQ和PI3K抑制剂处理的ZEA诱导的SCs细胞周期阻滞的影响。数据显示，ZEA可以通过将细胞周期阻滞在G2 / M期来抑制SC的增殖，并通过抑制PI3K / Akt / m TOR信号通路来触发自噬。促进或抑制自噬水平可以增强或逆转细胞周期的阻滞。并且它受PI3K / Akt / m TOR信号通路的调节。两者合计，这项研究提供的证据表明自噬和PI3K / Akt / m TOR信号通路参与调节由于ZEA在体外引起的大鼠原发性SCs细胞周期停滞。在某种程度上，ZEA诱导的自噬在此过程中起保护作用。

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