Airway pollution can affect the central nervous system, but whether this causes glial activation and inflammation in the nucleus of solitary tract (NTS) remains unclear. We used a rat model with exposure to diesel exhaust particulate matter (DEP) at 200 μg/m³ (low exposure) and 1000 μg/m³ (high exposure) for 14 days. Activation of microglia and astrocytes in the NTS was assessed using Iba-1 and glial fibrillary acidic protein (GFAP) staining. The expression of neurotrophic factors including brain-derived neurotrophic factor (BDNF), glial-derived neurotrophic factor (GDNF), and nerve growth factor (NGF) in the NTS were evaluated by immunofluorescence. Changes in the intracellular structure of NTS neurons were observed via electron microscopy. Inflammatory cytokines and oxidant stress levels in the medulla were also measured. Exposure to DEP can cause NTS inflammation as well as airway inflammation, especially in the H-exposure group. We showed that the numbers of microglia and astrocytes in the NTS, as well as NGF expression in the NTS, were significantly higher in both exposure groups than in controls, but BDNF or GDNF expression was not detected. Exposure to DEP induced ultrastructural changes in NTS neurons as reflected by endoplasmic reticulum dilation, ribosomal loss, mitochondrial vacuolization, and a sparse myelin sheath. Medulla inflammation and an imbalance of oxidants and antioxidants also resulted from exposure to DEP. The H-exposure group showed an imbalance of oxidants and antioxidants with decreased levels of SOD and GSH and increased levels of MDA and ROS compared to the control group (both p < 0.01) in the medulla. Inflammatory cytokines (IL-1β, IL-6, and TNF-α) were also significantly increased in the H-exposure group. Fourteen days of exposure to DEP can affect the NTS neurons in rat. Glial activation and inflammation may play important roles in the response of the NTS to DEP.

气道污染会影响中枢神经系统，但这是否会导致孤束核（NTS）中的胶质细胞活化和炎症仍不清楚。我们使用的大鼠模型暴露于200 μg/m ³ （低暴露）和1000 μg/m ³ （高暴露）的柴油机尾气颗粒物（DEP）14天。使用 Iba-1 和胶质纤维酸性蛋白 (GFAP) 染色评估 NTS 中小胶质细胞和星形胶质细胞的激活。通过免疫荧光法评估NTS中神经营养因子的表达，包括脑源性神经营养因子（BDNF）、胶质源性神经营养因子（GDNF）和神经生长因子（NGF）。通过电子显微镜观察NTS神经元细胞内结构的变化。还测量了髓质中的炎症细胞因子和氧化应激水平。暴露于 DEP 会导致 NTS 炎症和气道炎症，尤其是在 H 暴露组中。我们发现，两个暴露组的 NTS 中小胶质细胞和星形胶质细胞的数量以及 NGF 的表达均显着高于对照组，但未检测到 BDNF 或 GDNF 的表达。暴露于 DEP 会引起 NTS 神经元的超微结构变化，表现为内质网扩张、核糖体丢失、线粒体空泡化和髓鞘稀疏。髓质炎症以及氧化剂和抗氧化剂的不平衡也是由接触 DEP 引起的。与对照组相比，H暴露组髓质中氧化剂和抗氧化剂不平衡，SOD和GSH水平降低，MDA和ROS水平升高（均p < 0.01）。 在 H 暴露组中，炎症细胞因子（IL-1β、IL-6 和 TNF-α）也显着增加。暴露于 DEP 14 天可影响大鼠的 NTS 神经元。胶质细胞激活和炎症可能在 NTS 对 DEP 的反应中发挥重要作用。