Department of Pulmonary and Critical Care Medicine, Laboratory of Immunology, Affiliated Kunshan Hospital of Jiangsu University, Suzhou, Jiangsu, 215300, China; State Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong, 510120, China.
State Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong, 510120, China; Department of Pulmonary and Critical Care Medicine, Shantou Central Hospital, Affiliated Shantou Hospital of Sun Yat-sen University, Shantou, Guangdong, 515031, China.
Environ Toxicol Pharmacol. 2021 Apr;83:103584. doi: 10.1016/j.etap.2021.103584. Epub 2021 Jan 15.
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/m (low exposure) and 1000 μg/m (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.
大气污染会影响中枢神经系统，但这是否会导致孤束核（NTS）中的神经胶质细胞激活和炎症仍不清楚。我们使用了一种大鼠模型，该模型在 14 天内暴露于 200μg/m（低暴露）和 1000μg/m（高暴露）的柴油机排气颗粒物（DEP）中。通过 Iba-1 和胶质纤维酸性蛋白（GFAP）染色评估 NTS 中微胶质细胞和星形胶质细胞的激活。通过免疫荧光评估 NTS 中神经营养因子（包括脑源性神经营养因子（BDNF）、胶质细胞源性神经营养因子（GDNF）和神经生长因子（NGF）的表达。通过电子显微镜观察 NTS 神经元的细胞内结构变化。还测量了延髓中炎症细胞因子和氧化应激水平。DEP 暴露会引起 NTS 炎症和气道炎症，尤其是在 H 暴露组中。我们表明，NTS 中的小胶质细胞和星形胶质细胞数量以及 NTS 中的 NGF 表达在两个暴露组中均明显高于对照组，但未检测到 BDNF 或 GDNF 表达。DEP 暴露导致 NTS 神经元的超微结构发生变化，表现为内质网扩张、核糖体丢失、线粒体空泡化和髓鞘稀疏。DEP 暴露还导致延髓炎症和氧化还原失衡。与对照组相比，H 暴露组中 SOD 和 GSH 水平降低，MDA 和 ROS 水平升高，表明氧化还原失衡（均 p < 0.01）。H 暴露组中的炎性细胞因子（IL-1β、IL-6 和 TNF-α）也显著增加。14 天 DEP 暴露可影响大鼠 NTS 神经元。胶质细胞激活和炎症可能在 NTS 对 DEP 的反应中起重要作用。
