Lee Sun Hwa, Yang Eun Jin
Department of Clinical Research, Korea Institute of Oriental Medicine, 1672 Yuseong-daero, Yuseong-gu, Daejeon 305-811, Republic of Korea.
Evid Based Complement Alternat Med. 2019 Feb 12;2019:1893526. doi: 10.1155/2019/1893526. eCollection 2019.
Neuroinflammation is considered a critical factor in the pathologic mechanisms of amyotrophic lateral sclerosis (ALS). This study examined the levels of neuroinflammatory proteins in the spinal cord of JGT-treated transgenic mice to determine the effect of Jaeumganghwa-Tang (JGT) on neuroinflammation. Twelve 8-week-old male experimental mice were randomly allocated to three groups: a non-transgenic group, a hSOD1 transgenic group, and a hSOD1 transgenic group that received JGT 1 mg/g orally once daily for 6 weeks. After 6 weeks, the spinal cord tissues were analyzed for inflammatory proteins (Iba-1, toll-like receptor 4, and tumor necrosis factor-) and oxidative stress-related proteins (transferrin, ferritin, HO1, and NQO1) by Western blot analysis. Administration of JGT significantly delayed motor function impairment and reduced oxidative stress in transgenic mice. JGT effectively ameliorated neuroinflammation mechanisms by downregulating TLR4-related signaling proteins and improving iron homeostasis in the spinal cord of mice. JGT could help to decrease neuroinflammation and protect neuronal cells by strengthening the immune response in the central nervous system. This is the first study to demonstrate the role of JGT in neuroinflammation in an animal model of ALS.
神经炎症被认为是肌萎缩侧索硬化症（ALS）病理机制中的一个关键因素。本研究检测了经Jaeumganghwa-Tang（JGT）处理的转基因小鼠脊髓中神经炎症蛋白的水平，以确定Jaeumganghwa-Tang（JGT）对神经炎症的影响。将12只8周龄雄性实验小鼠随机分为三组：非转基因组、hSOD1转基因组和hSOD1转基因组，后者每天口服1mg/g JGT，持续6周。6周后，通过蛋白质免疫印迹分析检测脊髓组织中的炎症蛋白（离子钙接头蛋白1、Toll样受体4和肿瘤坏死因子-α）和氧化应激相关蛋白（转铁蛋白、铁蛋白、血红素加氧酶1和醌氧化还原酶1）。给予JGT可显著延缓转基因小鼠的运动功能损害并降低氧化应激。JGT通过下调TLR4相关信号蛋白和改善小鼠脊髓中的铁稳态，有效改善了神经炎症机制。JGT可以通过增强中枢神经系统的免疫反应来帮助减轻神经炎症并保护神经元细胞。这是第一项在ALS动物模型中证明JGT在神经炎症中作用的研究。
