Cao Junhan, Yao Mengke, Wang Kai, Qin Ling, Zhang Qing, Zhang Haibo, Wei Jinzheng, Qu Changfeng, Xue Changhu, Miao Jinlai
College of Food Science and Engineering, Ocean University of China, Qingdao 266003, China.
Qingdao Key Laboratory of Marine Natural Products Research and Development Laboratory, First Institute of Oceanography, Ministry of Natural Resources, Qingdao 266061, China.
J Agric Food Chem. 2025 Jun 11;73(23):14333-14352. doi: 10.1021/acs.jafc.5c02190. Epub 2025 May 30.
Antibiotic-based eradication therapy for faces challenges such as the increasing number of antibiotic-resistant strains and gut microbiota dysbiosis. The study evaluated the effects of fucoidan from sea cucumber cooking liquid (Fuc-SC) on (Hp SS1)-associated gastritis. The backbone structure of Fuc-SC was composed of alternating → 3)-α-L-Fuc-(1 → 4)-α-L-Fuc-(1 → linked fucose residues. The mouse experiments demonstrated that Fuc-SC reduced the colonization of Hp SS1 in the gastric mucosa through decreasing the level of urease, Hp-IgG, and CagA-IgG. In addition, Fuc-SC regulated oxidative stress levels by reducing NO, MDA, and ROS levels, while increasing the activity of SOD and GSH-Px. Compared to antibiotic treatment alone, the combination of Fuc-SC with antibiotics further enhanced the antioxidant effects. Molecular mechanisms indicated that Fuc-SC regulated the MAPK/NF-κB signaling pathway, downregulating the expression of inflammatory factors such as IL-1β and TNF-α and further modulating the expression of S100A8 and E-cadherin. Gut microbiota analysis indicated that Fuc-SC reversed the depletion of caused by antibiotic treatment. Additionally, Fuc-SC significantly promoted the biosynthesis of microbial metabolites such as butyric acid, isobutyric acid, hexanoic acid, and phospholipids, thereby alleviating inflammation. These findings highlight its potential as a sustainable, nonantibiotic therapy for -associated gastritis.
基于抗生素的根除疗法面临着诸如抗生素耐药菌株数量增加和肠道微生物群失调等挑战。该研究评估了海参蒸煮液中的岩藻聚糖（Fuc-SC）对幽门螺杆菌（Hp SS1）相关性胃炎的影响。Fuc-SC的主链结构由交替的→3)-α-L-岩藻糖-(1→4)-α-L-岩藻糖-(1→连接的岩藻糖残基组成。小鼠实验表明，Fuc-SC通过降低脲酶、Hp-IgG和CagA-IgG水平，减少了Hp SS1在胃黏膜中的定植。此外，Fuc-SC通过降低NO、MDA和ROS水平，同时增加SOD和GSH-Px的活性来调节氧化应激水平。与单独使用抗生素治疗相比，Fuc-SC与抗生素联合使用进一步增强了抗氧化作用。分子机制表明，Fuc-SC调节MAPK/NF-κB信号通路，下调IL-1β和TNF-α等炎症因子的表达，并进一步调节S100A8和E-钙黏蛋白的表达。肠道微生物群分析表明，Fuc-SC逆转了抗生素治疗引起的某种微生物的减少。此外，Fuc-SC显著促进了丁酸、异丁酸、己酸和磷脂等微生物代谢产物的生物合成，从而减轻了炎症。这些发现突出了其作为幽门螺杆菌相关性胃炎的可持续、非抗生素疗法的潜力。
