Dietary fiber is named as “the 7th nutrient” for humans, which is beneficial to improve intestinal health and prevent metabolic disease of the host. Mechanisms of dietary fiber administration on improved host health are mediated by short chain fatty acids (SCFA), which are reported to activate G protein-coupled receptors (GPR) and suppress activity of histone deacetylase (HDAC) to down-regulate expression of nuclear factor-к-gene binding (NF-кB) signaling. Arabinoxylan is fermented by gut microbiota to produce SCFA and improved microbial community composition, intestinal barrier functions and host health. Interestingly, the latest publications have observed that ferulic acid combined with the arabinose in arabinoxylans from various cereal grains can be released through gut microbial fermentation. Ferulic acid can improve antioxidase activity and decrease reactive oxygen species (ROS) concentration by activating the signaling pathway of Kelch-like ECH-associated protein-1 and nuclear factor E2-related factor-2 (Keap1-Nrf2). However, the role of ferulic acid in cooperation with SCFA produced from microbial fermentation of cereal-derived arabinoxylan to regulate the intestinal health and host metabolisms, has been widely unclear. This review summarizes the potential mechanisms of ferulic acid from microbial fermentation of cereal-derived arabinoxylans on immunological functions and physiological metabolisms of the host. The evidence presented in the review indicates that dietary supplementation with cereal-derived arabinoxylans improves antioxidant capacity of intestinal epithelial cells due to the production of ferulic acid and SCFA from microbial fermentation. Ferulic acid can cooperate with SCFA to regulate intestinal integrity and immunological functions of the host. Peroxisome proliferator activated-receptor γ (PPARγ) may play an important role in integrating ferulic acid and SCFA to regulate host health and metabolism.

膳食纤维被称为人体的“第七大营养素”，有利于改善肠道健康，预防宿主代谢性疾病。膳食纤维改善宿主健康的机制是由短链脂肪酸 (SCFA) 介导的，据报道其激活 G 蛋白偶联受体 (GPR) 并抑制组蛋白脱乙酰酶 (HDAC) 的活性以下调核因子的表达-к-基因结合（NF-кB）信号。阿拉伯木聚糖被肠道微生物群发酵以产生 SCFA 并改善微生物群落组成、肠道屏障功能和宿主健康。有趣的是，最新的出版物观察到阿魏酸与来自各种谷物的阿拉伯木聚糖中的阿拉伯糖结合可以通过肠道微生物发酵释放。阿魏酸可通过激活 Kelch 样 ECH 相关蛋白 1 和核因子 E2 相关因子 2 (Keap1-Nrf2) 的信号通路来提高抗氧化酶活性并降低活性氧 (ROS) 浓度。然而，阿魏酸与由谷物衍生的阿拉伯木聚糖微生物发酵产生的 SCFA 协同作用以调节肠道健康和宿主代谢的作用尚不清楚。本综述总结了谷源性阿拉伯木聚糖微生物发酵产生的阿魏酸对宿主免疫功能和生理代谢的潜在作用机制。审查中提供的证据表明，由于微生物发酵产生阿魏酸和 SCFA，膳食中添加谷物衍生的阿拉伯木聚糖可提高肠上皮细胞的抗氧化能力。阿魏酸可与 SCFA 协同调节宿主的肠道完整性和免疫功能。过氧化物酶体增殖物激活受体 γ (PPARγ) 可能在整合阿魏酸和 SCFA 以调节宿主健康和新陈代谢方面发挥重要作用。