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目的研究三邻甲苯磷酸酯(TOCP)所致迟发性神经病(OPIDN)中AKT/mTOR/p70S6K信号通路的变化,探讨OPIDN发生的分子机制。方法 30只成年罗曼母鸡随机分为5组,每组6只,给予750 mg/kg TOCP一次性灌胃,然后分别在TOCP染毒后0、1、5、10和21 d时间点处死一组动物取脊髓组织,免疫印迹法检测脊髓中AKT、p-AKT、p70S6K、p-p70S6K和mTOR的相对含量。结果 TOCP染毒引起母鸡脊髓中磷酸化AKT、p70S6K和mTOR的含量显著下降(P<0.05),而AKT、p70S6K的含量没有明显变化(P>0.05)。结论 TOCP干扰了AKT/mTOR/p70S6K信号通路的调节机制,这可能与OPIDN的发病机制有关。
Objective To investigate the changes of AKT / mTOR / p70S6K signaling pathway in delayed neuropathies (OPIDN) induced by trioctylphosphate (TOCP) and to explore the molecular mechanism of OPIDN. Methods Thirty adult roman hens were randomly divided into five groups with 6 mice in each group. The animals were given 750 mg / kg TOCP once a day for gavage, then sacrificed at 0, 1, 5, 10 and 21 d after TOCP exposure The spinal cord tissues were taken from the animals and the relative contents of AKT, p-AKT, p70S6K, p-p70S6K and mTOR in the spinal cord were detected by immunoblotting. Results The levels of phosphorylated AKT, p70S6K and mTOR in the spinal cord of TOCP-treated mice were significantly decreased (P <0.05), while the contents of AKT and p70S6K did not change significantly (P> 0.05). Conclusion TOCP interferes with the regulatory mechanism of AKT / mTOR / p70S6K signaling pathway, which may be related to the pathogenesis of OPIDN.