Qin Ningbo, Liu Hongxu, Wang Xinru, Liu Yi, Chang Hong, Xia Xiaodong
SKL of Marine Food Processing & Safety Control, National Engineering Research Center of Seafood, School of Food Science and Technology, Dalian Polytechnic University, Dalian 116034, China.
SKL of Marine Food Processing & Safety Control, National Engineering Research Center of Seafood, School of Food Science and Technology, Dalian Polytechnic University, Dalian 116034, China.
Int J Biol Macromol. 2025 Apr;300:140271. doi: 10.1016/j.ijbiomac.2025.140271. Epub 2025 Jan 23.
Sargassum fusiforme, widely consumed in Asian countries, has been proven to have various biological activities. However, the impacts and mechanisms of Sargassum fusiforme polysaccharides (SFPs) on intestinal bacterial infection are not yet fully understood. Our findings indicate that SFPs pretreatment ameliorates intestinal inflammation by reducing C. rodentium colonization, increasing colon length and levels of IL-10 and IL-22, decreasing IL-1β, IL-6, TNF-α, and IL-17 levels, inhibiting colonic crypt elongation and hyperplasia, and enhancing the intestinal mucosal barrier. The protective effects against intestinal bacterial infection are linked to enhanced clearance of C. rodentium and improvements in the intestinal mucosal barrier and C. rodentium-induced intestinal microbiota dysbiosis. Fecal microbiota transplantation experiments were conducted to evaluate the functional impact of microbiota induced by SFPs. The results suggest that intestinal microbiota modified by SFPs effectively countered C. rodentium infection. In addition, our study identified that miRNA-92a-3p is partially complementary to the 3'-UTR of the Notch1 gene, thereby repressing the Notch1-Hes1 signaling pathway and enhancing Muc2 secretion. Taken together, these findings reveal that SFPs protect mice from C. rodentium infection by activating the miR-92a-3p/Notch1-Hes1 regulatory axis driven by the intestinal microbiota, which stimulates Muc2 production to maintain intestinal barrier homeostasis.
羊栖菜在亚洲国家被广泛食用，已被证明具有多种生物活性。然而，羊栖菜多糖（SFPs）对肠道细菌感染的影响及机制尚未完全明确。我们的研究结果表明，SFPs预处理可通过减少鼠柠檬酸杆菌的定植、增加结肠长度以及IL-10和IL-22水平、降低IL-1β、IL-6、TNF-α和IL-17水平、抑制结肠隐窝延长和增生以及增强肠道黏膜屏障来改善肠道炎症。对肠道细菌感染的保护作用与增强鼠柠檬酸杆菌的清除以及改善肠道黏膜屏障和鼠柠檬酸杆菌诱导的肠道微生物群失调有关。进行了粪便微生物群移植实验以评估SFPs诱导的微生物群的功能影响。结果表明，经SFPs修饰的肠道微生物群有效对抗了鼠柠檬酸杆菌感染。此外，我们的研究发现miRNA-92a-3p与Notch1基因的3'-UTR部分互补，从而抑制Notch1-Hes1信号通路并增强Muc2分泌。综上所述，这些发现揭示了SFPs通过激活由肠道微生物群驱动的miR-92a-3p/Notch1-Hes1调节轴来保护小鼠免受鼠柠檬酸杆菌感染，该调节轴刺激Muc2产生以维持肠道屏障稳态。
