Department of Food and Nutrition, Kyung Hee University, Seoul 02447, Korea.
Neurobiota Research Center, College of Pharmacy, Kyung Hee University, Seoul 02447, Korea.
Nutrients. 2020 Nov 10;12(11):3441. doi: 10.3390/nu12113441.
Excessive expression of interleukin (IL)-1β in the brain causes depression and cognitive dysfunction. Herein, we investigated the effect of NK109, which suppressed IL-1β expression in activated macrophages, on K1-induced cognitive impairment and depression in mice. Germ-free and specific pathogen-free mice with neuropsychiatric disorders were prepared by oral gavage of K1. NK109 alleviated K1-induced cognition-impaired and depressive behaviors, decreased the expression of IL-1β and populations of NF-κB/Iba1 and IL-1R cells, and increased the K1-suppressed population of BDNF/NeuN cells in the hippocampus. However, its effects were partially attenuated by celiac vagotomy. NK109 treatment mitigated K1-induced colitis and gut dysbiosis. Tyndallized NK109, even if lysed, alleviated cognitive impairment and depression. In conclusion, NK109 alleviated neuropsychiatric disorders and colitis by modulating IL-1β expression, gut microbiota, and vagus nerve-mediated gut-brain signaling.
白细胞介素 (IL)-1β 在大脑中的过度表达会导致抑郁和认知功能障碍。在此，我们研究了 NK109 的作用，它可抑制活化巨噬细胞中 IL-1β 的表达。NK109 减轻了 K1 诱导的小鼠认知障碍和抑郁行为，降低了 IL-1β 和 NF-κB/Iba1 和 IL-1R 细胞的表达，并增加了海马中 K1 抑制的 BDNF/NeuN 细胞的数量。然而，其作用部分被腹腔迷走神经切断术减弱。NK109 治疗减轻了 K1 诱导的结肠炎和肠道菌群失调。Tyndallized NK109，即使裂解，也能减轻认知障碍和抑郁。总之，NK109 通过调节 IL-1β 表达、肠道微生物群和迷走神经介导的肠脑信号来缓解神经精神疾病和结肠炎。
