Department of Food and Nutrition, Kyung Hee University, Seoul 02447, Republic of Korea.
Neurobiota Research Center, College of Pharmacy, Kyung Hee University, Seoul 02447, Republic of Korea.
Nutrients. 2023 Feb 3;15(3):790. doi: 10.3390/nu15030790.
Aging-related gut microbiota dysbiosis initiates gut inflammation and microbiota dysbiosis, which induce the occurrence of psychiatric disorders including dementia. The alleviation of gut microbiota dysbiosis by probiotics is suggested to be able to alleviate psychiatric disorders including cognitive impairment (CI). Therefore, to understand how probiotics could alleviate CI, we examined the effects of anti-inflammatory NK109 and its supplement (NS, mixture of NK109 and soybean embryo ethanol extract) on cognitive function in aged (Ag), 5XFAD transgenic (Tg), or mildly cognition-impaired adult fecal microbiota (MCF)-transplanted mice. Oral administration of NK109 or NS decreased CI-like behaviors in Ag mice. Their treatments suppressed TNF-α and p16 expression and NF-κB-activated cell populations in the hippocampus and colon, while BDNF expression was induced. Moreover, they partially shifted the β-diversity of gut microbiota in Ag mice to those of young mice: they decreased Bifidobacteriaceae, Lactobacillaceae, and Helicobacteriaceae populations and increased Rikenellaceae and Prevotellaceae populations. Oral administration of NK109 or NS also reduced CI-like behaviors in Tg mice. Their treatments induced BDNF expression in the hippocampus, decreased hippocampal TNF-α and Aβ expression and hippocampal and colonic NF-κB-activated cell populations. NK109 and NS partially shifted the β-diversity of gut microbiota in Tg mice: they decreased Muribaculaceae and Rhodospiraceae populations and increased Helicobacteriaceae population. Oral administration of NK109 or NS decreased MCF transplantation-induced CI-like behaviors in mice. NK109 and NS increased hippocampal BDNF expression, while hippocampal and colonic TNF-α expression and NF-κB-activated cell populations decreased. These findings suggest that dementia can fluctuate the gut microbiota composition and NK109 and its supplement NS can alleviate CI with systemic inflammation by inducing BDNF expression and suppressing NF-κB activation and gut microbiota dysbiosis.
衰老相关的肠道微生物群落失调会引发肠道炎症和微生物群落失调，从而导致包括痴呆症在内的精神疾病的发生。益生菌缓解肠道微生物群落失调被认为能够缓解包括认知障碍（CI）在内的精神疾病。因此，为了了解益生菌如何缓解 CI，我们研究了抗炎 NK109 及其补充剂（NS，NK109 和大豆胚胎乙醇提取物的混合物）对老年（Ag）、5XFAD 转基因（Tg）或轻度认知障碍成年粪便微生物群（MCF）移植小鼠认知功能的影响。NK109 或 NS 的口服给药可降低 Ag 小鼠的 CI 样行为。它们的治疗抑制了海马体和结肠中 TNF-α 和 p16 的表达以及 NF-κB 激活的细胞群，同时诱导了 BDNF 的表达。此外，它们部分改变了 Ag 小鼠的肠道微生物群落 β 多样性，使其向年轻小鼠的肠道微生物群落转变：它们降低了双歧杆菌科、乳杆菌科和螺旋杆菌科的种群，增加了 Rikenellaceae 和 Prevotellaceae 的种群。NK109 或 NS 的口服给药也降低了 Tg 小鼠的 CI 样行为。它们的治疗诱导了海马体中的 BDNF 表达，降低了海马体和结肠中的 TNF-α 和 Aβ 表达以及海马体和结肠中的 NF-κB 激活的细胞群。NK109 和 NS 部分改变了 Tg 小鼠的肠道微生物群落 β 多样性：它们降低了 Muribaculaceae 和 Rhodospiraceae 的种群，增加了螺旋杆菌科的种群。NK109 和 NS 的口服给药降低了 MCF 移植诱导的小鼠 CI 样行为。NK109 和 NS 增加了海马体中的 BDNF 表达，同时降低了海马体和结肠中的 TNF-α 表达和 NF-κB 激活的细胞群。这些发现表明，痴呆症可以改变肠道微生物群落的组成，而 NK109 和其补充剂 NS 可以通过诱导 BDNF 表达和抑制 NF-κB 激活和肠道微生物群落失调来缓解全身性炎症引起的 CI。
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