Kang Jin-Yong, Kim Jong-Min, Park Seon-Kyeong, Lee Hyo-Lim, Heo Ho-Jin
Division of Applied Life Science (BK21), Institute of Agriculture and Life Science, Gyeongsang National University, Jinju 52828, Republic of Korea.
Research and Development Division, World Institute of Kimchi, Gwangju 61755, Republic of Korea.
Plants (Basel). 2023 Mar 8;12(6):1230. doi: 10.3390/plants12061230.
This study was performed to investigate the improving effect of a mixture of and (AASC) on cognitive dysfunction in mice with long-term exposure to fine particles (particulate matter smaller than 2.5 µm: PM). The main compounds of AASC were identified as dicaffeoylquinic acid isomers of and a quercetin-3-glucoside of . As a result of behavioral tests for the evaluation of cognitive function, it was confirmed that cognitive dysfunction was induced in the PM exposure group, and a tendency to improve in the AASC group was confirmed. Increased oxidative stress and inflammatory response and mitochondrial dysfunction were observed in the brain and lung tissues of the PM group. Damage to the brain and lung affected the accumulation of amyloid beta (Aβ) in the brain. It increased Aβ and induced the cholinergic dysfunction, hyperphosphorylation of the tau protein, and activation of apoptosis, leading to cognitive impairment. However, AASC suppressed brain and lung oxidative stress and inflammation, thereby suppressing brain Aβ expression. Consequently, this study shows the potential that a steady intake of plant resources with antioxidant and anti-inflammatory activity could prevent cognitive impairment caused by PM.
本研究旨在探讨刺五加和黄芪混合物（AASC）对长期暴露于细颗粒物（小于2.5微米的颗粒物：PM）的小鼠认知功能障碍的改善作用。AASC的主要化合物被鉴定为刺五加的二咖啡酰奎尼酸异构体和黄芪的槲皮素-3-葡萄糖苷。通过行为测试评估认知功能，证实PM暴露组诱导了认知功能障碍，且AASC组有改善趋势。在PM组的脑和肺组织中观察到氧化应激增加、炎症反应和线粒体功能障碍。脑和肺的损伤影响了脑中β淀粉样蛋白（Aβ）的积累。它增加了Aβ并诱导胆碱能功能障碍、tau蛋白的过度磷酸化和细胞凋亡的激活，导致认知障碍。然而，AASC抑制了脑和肺的氧化应激和炎症，从而抑制了脑Aβ表达。因此，本研究表明，持续摄入具有抗氧化和抗炎活性的植物资源有可能预防PM引起的认知障碍。
