A growing body of evidence indicates that exposure to nonylphenol (NP), a typical persistent organic pollutant (POP), in early life results in the impairment of the central nervous system (CNS), but the underlying mechanism still remains to be elucidated. High levels of pro-inflammatory cytokines in the brain have been implicated in the CNS damages. The animal model of exposure to NP in early life was established by maternal gavage during the pregnancy and lactation in the present study. We found that exposure to NP in early life increased the levels of pro-inflammatory cytokines in the rat prefrontal cortex. Interestingly, the levels of pro-inflammatory cytokines in the intestine as well as in the serum were also increased by NP exposure. Furthermore, the increased permeability of intestinal barrier and blood-brain barrier (BBB), two critical barriers in the gut to brain communication, was observed in the rats exposed to NP in early lives. The decreased expression of zonula occludens-1 (ZO-1) and claudin-1 (CLDN-1), tight junction proteins (TJs) that responsible for maintaining the permeability of intestinal barrier and BBB, was found, which may underlie these increases in permeability. Taken together, these results suggested that the disturbed gut-brain communication may contribute to the increased levels of pro-inflammatory cytokines in the prefrontal cortex caused by NP exposure in early life.

中文翻译：

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早年暴露于壬基酚会增加前额叶皮层的促炎细胞因子：肠脑沟通的参与。

越来越多的证据表明，早年接触壬基酚（NP）（一种典型的持久性有机污染物（POP））会导致中枢神经系统（CNS）受损，但其潜在机制仍有待阐明。脑中高水平的促炎细胞因子与中枢神经系统损害有关。在本研究中，通过孕期和哺乳期的母亲管饲法建立了早期暴露于NP的动物模型。我们发现，在生命早期暴露于NP会增加大鼠前额叶皮层中促炎性细胞因子的水平。有趣的是，NP暴露也增加了肠道以及血清中促炎细胞因子的水平。此外，肠屏障和血脑屏障（BBB）的通透性增加，在生命早期暴露于NP的大鼠中观察到了肠道中两个重要的障碍，阻碍了大脑的交流。发现负责维持肠屏障和BBB通透性的紧密连接蛋白（TJ）的小带闭合蛋白1（ZO-1）和claudin-1（CLDN-1）的表达降低，这可能是这些增加的原因。渗透性。综上所述，这些结果表明，肠蠕动障碍可能是由于早期暴露于NP导致前额叶皮层促炎性细胞因子水平升高的原因。已发现负责维持肠屏障和BBB通透性的紧密连接蛋白（TJs），可能是这些通透性增加的基础。综上所述，这些结果表明，肠蠕动障碍可能是由于早期暴露于NP导致前额叶皮层促炎性细胞因子水平升高的原因。已发现负责维持肠屏障和BBB通透性的紧密连接蛋白（TJ），这可能是这些通透性增加的基础。综上所述，这些结果表明，肠蠕动障碍可能是由于早期暴露于NP导致前额叶皮层促炎性细胞因子水平升高的原因。