Wu Zhifeng, He Jinhui, Zhang Zeyue, Li Jingjing, Zou Huicong, Tan Xiang, Wang Yuqing, Yao Yong, Xiong Wen
College of Animal Sciences and Technology and College of Veterinary Medicine, Huazhong Agricultural University, Wuhan 430070, China.
J Agric Food Chem. 2023 Oct 18;71(41):14951-14966. doi: 10.1021/acs.jafc.3c00278. Epub 2023 Oct 3.
In this study, we investigated the effects of on the mouse colitis model. The results showed that the supernatant of the culture alleviated colitis and remodeled gut microbiota, represented by an increased abundance of bacteria producing short-chain fatty acids, leading to an increased concentration of propionic acid in the intestine. Further studies revealed that propionic acid inhibited activation of the MAPK signaling pathway and polarization of M1 macrophages. Macrophage clearance assays confirmed that macrophages are indispensable for alleviating colitis through propionic acid. experiments showed that propionic acid directly inhibited the MAPK signaling pathway in macrophages and reduced M1 macrophage polarization, thereby inhibiting the secretion of pro-inflammatory cytokines. These findings improve our understanding of how attenuates inflammatory bowel disease (IBD) and provide valuable insights for identifying molecular targets for IBD treatment in the future.
在本研究中,我们调查了[具体物质]对小鼠结肠炎模型的影响。结果表明,[具体物质]培养物的上清液减轻了结肠炎并重塑了肠道微生物群,表现为产生短链脂肪酸的细菌丰度增加,导致肠道中丙酸浓度升高。进一步研究表明,丙酸抑制丝裂原活化蛋白激酶(MAPK)信号通路的激活和M1巨噬细胞的极化。巨噬细胞清除试验证实,巨噬细胞对于通过丙酸减轻结肠炎是必不可少的。[具体]实验表明,丙酸直接抑制巨噬细胞中的MAPK信号通路并减少M1巨噬细胞极化,从而抑制促炎细胞因子的分泌。这些发现增进了我们对[具体物质]如何减轻炎症性肠病(IBD)的理解,并为未来确定IBD治疗的分子靶点提供了有价值的见解。