We have reported that smoking during pregnancy is associated with deficit in neonatal central chemoreception. However, the underlying mechanism is not well clarified. In this study, we developed a rat model of maternal cigarette smoke (CS) exposure. Pregnant rats were exposed to CS during gestational day 1−20. Offspring were studied on postnatal day 2. Reactive oxygen species (ROS) content and expressions of antioxidant proteins in retrotrapezoid nucleus/parafacial respiratory group (RTN/pFRG) were examined by fluorogenic dye MitoSOX™ Red and Western blotting, respectively. The response of hypoglossal rootlets discharge to acidification was also detected with micro-injection of H₂O₂ into RTN/pFRG of offspring brainstem slices in vitro. Results showed that maternal CS exposure led to an increase in ROS production, and brought about decreases in mitochondrial superoxide dismutase and Kelch-like ECH-associated protein-1, and an increase in NF-E2-related factor 2 in offspring RTN/pFRG. Catalase and glutathione reductase expressions were not significantly changed. Moreover, oxidative stress induced by micro-injection of H₂O₂ into RTN/pFRG in vitro inhibited the discharge response of hypoglossal rootlets to acidification. These findings suggest that maternal CS exposure results in oxidative stress in RTN/pFRG of rat offspring, which might play a role in the impairment of central chemoreception.

我们已经报告说，怀孕期间吸烟与新生儿中枢化学感受的缺陷有关。然而，潜在的机制并没有得到很好的阐明。在这项研究中，我们开发了母体香烟烟雾 (CS) 暴露的大鼠模型。妊娠大鼠在妊娠第 1-20 天暴露于 CS。在出生后第 2 天对后代进行研究。分别通过荧光染料 MitoSOX™ Red 和蛋白质印迹检查后梯形核/面旁呼吸组 (RTN/pFRG) 中活性氧 (ROS) 的含量和抗氧化蛋白的表达。在体外将H ₂ O ₂微量注射到子代脑干切片的RTN/pFRG中也检测了舌下根放电对酸化的反应. 结果表明，母体 CS 暴露导致 ROS 产生增加，并导致线粒体超氧化物歧化酶和 Kelch 样 ECH 相关蛋白-1 减少，以及后代 RTN/pFRG 中 NF-E2 相关因子 2 增加。过氧化氢酶和谷胱甘肽还原酶的表达没有显着变化。此外，体外将H ₂ O ₂微量注射到RTN/pFRG中诱导的氧化应激抑制了舌下小根对酸化的放电反应。这些发现表明母体 CS 暴露导致大鼠后代 RTN/pFRG 的氧化应激，这可能在中枢化学感受的损害中起作用。