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Mechanistic basis and preliminary practice of butyric acid and butyrate sodium to mitigate gut inflammatory diseases: a comprehensive review
Nutrition Research ( IF 3.4 ) Pub Date : 2021-09-09 , DOI: 10.1016/j.nutres.2021.08.007
Mingbao Zhang 1 , Yanan Wang 1 , Xianqi Zhao 2 , Chang Liu 2 , Baozhen Wang 3 , Jun Zhou 3
Affiliation  

A key event featured in the early stage of chronic gut inflammatory diseases is the disordered recruitment and excess accumulation of immune cells in the gut lamina propria. This process is followed by the over-secretion of pro-inflammatory factors and the prolonged overactive inflammatory responses. Growing evidence has suggested that gut inflammatory diseases may be mitigated by butyric acid (BA) or butyrate sodium (NaB). Laboratory studies show that BA and NaB can enhance gut innate immune function through G-protein-mediated signaling pathways while mitigating the overactive inflammatory responses by inhibiting histone deacetylase. The regulatory effects may occur in both epithelial enterocytes and the immune cells in the lamina propria. Prior to further clinical trials, comprehensive literature reviews and rigid examination concerning the underlying mechanism are necessary. To this end, we collected and reviewed 197 published reports regarding the mechanisms, bioactivities, and clinical effects of BA and NaB to modulate gut inflammatory diseases. Our review found insufficient evidence to guarantee the safety of clinical practice of BA and NaB, either by anal enema or oral administration of capsule or tablet. The safety of clinical use of BA and NaB should be further evaluated. Alternatively, dietary patterns rich in “fruits, vegetables and beans” may be an effective and safe approach to prevent gut inflammatory disease, which elevates gut microbiota-dependent production of BA. Our review provides a comprehensive reference to future clinical trials of BA and NaB to treat gut inflammatory diseases.



中文翻译:

丁酸丁酸钠减轻肠道炎性疾病的机制基础及初步实践:综合评述

慢性肠道炎性疾病早期的一个关键事件是肠道固有层中免疫细胞的无序募集和过度积累。这个过程之后是促炎因子的过度分泌和长期过度活跃的炎症反应。越来越多的证据表明,丁酸 (BA) 或丁酸钠 (NaB) 可以缓解肠道炎症性疾病。实验室研究表明,BA 和 NaB 可以通过 G 蛋白介导的信号通路增强肠道先天免疫功能,同时通过抑制组蛋白脱乙酰酶来减轻过度活跃的炎症反应。调节作用可能发生在上皮肠细胞和固有层中的免疫细胞中. 在进一步的临床试验之前,有必要对潜在机制进行全面的文献回顾和严格检查。为此,我们收集并回顾了 197 篇已发表的关于 BA 和 NaB 调节肠道炎症性疾病的机制、生物活性和临床效果的报告。我们的审查发现没有足够的证据来保证 BA 和 NaB 临床实践的安全性,无论是通过肛门灌肠还是口服胶囊或片剂。应进一步评估 BA 和 NaB 临床使用的安全性。或者,富含“水果、蔬菜和豆类”的饮食模式可能是预防肠道炎症性疾病的一种有效且安全的方法,这会提高肠道微生物群依赖性 BA 的产生。

更新日期:2021-10-30
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