Li Yansong, Yang Zhangsheng, Liu Bin, Valdez Celina, Chavko Mikulas, Cancio Leopoldo C
US Army Institute of Surgical Research, 3698 Chambers Pass, Fort Sam Houston, TX.
Naval Medical Research Center, 503 Robert Grant Avenue, Silver Spring, MD.
Mil Med. 2019 Mar 1;184(Suppl 1):265-272. doi: 10.1093/milmed/usy330.
Mild blast traumatic brain injury is commonly prevalent in modern combat casualty care and has been associated with the development of neurodegenerative conditions. However, whether primary lower level blast overpressure (LBOP) causes neurodegeneration and neuroinflammation remains largely unknown. The aim of our present study was to determine whether LBOP can cause neuroinflammation and neurodegeneration.
Anesthetized rats were randomly assigned to LBOP group (70 kPa, n = 5) or sham group (without blast, n = 5). Histopathological and cytokine changes in brain tissue at 5 days post-injury were evaluated by hematoxylin-eosin staining and Bioplex assay, respectively.
Histopathological assessment revealed neuronal degeneration and increased density of inflammatory cells in frontal and parietal cortex, hippocampus and thalamus in rats exposed to LBOP. LBOP exposure significantly elevated levels of pro-inflammatory cytokines (EPO, IL-1β, IL-6, IL-12, IL-18, and TNF-α) and chemokines (GRO and RANTES) as well as of an anti-inflammatory cytokine (IL-13) in the frontal cortex.
This study reveals a role of neuroinflammation in neurodegeneration after mild blast traumatic brain injury. Therapies that target this process might in warfighters might function either by attenuating the development of post-traumatic stress disorder, chronic traumatic encephalopathy and Alzheimer's disease, or by slowing their progression.
轻度爆炸性创伤性脑损伤在现代战斗伤员护理中普遍存在，并与神经退行性疾病的发展有关。然而，原发性较低水平的爆炸超压（LBOP）是否会导致神经退行性变和神经炎症在很大程度上仍不清楚。我们目前研究的目的是确定LBOP是否会导致神经炎症和神经退行性变。
将麻醉大鼠随机分为LBOP组（70 kPa，n = 5）或假手术组（无爆炸，n = 5）。分别通过苏木精-伊红染色和生物芯片分析评估损伤后5天脑组织中的组织病理学和细胞因子变化。
组织病理学评估显示，暴露于LBOP的大鼠额叶、顶叶皮质、海马体和丘脑中存在神经元变性，炎症细胞密度增加。暴露于LBOP显著提高了额叶皮质中促炎细胞因子（EPO、IL-1β、IL-6、IL-12、IL-18和TNF-α）、趋化因子（GRO和RANTES）以及抗炎细胞因子（IL-13）的水平。
本研究揭示了神经炎症在轻度爆炸性创伤性脑损伤后神经退行性变中的作用。针对这一过程的治疗方法可能对战士有效，要么通过减轻创伤后应激障碍、慢性创伤性脑病和阿尔茨海默病的发展，要么通过减缓其进展。
