Fucoidan is a sulfated polysaccharide derived from brown algae (Saccharina japonica), and exhibits immunomodulatory properties. Emerging evidence suggests a strong correlation between the development of food allergy and intestinal dysfunction. The present study aimed to investigate the potential anti-food allergy activity of fucoidan and to elucidate its mechanism at the intestinal barrier function. The ovalbumin (OVA)-induced allergy mouse model was established, exhibiting increased OVA-specific IgE, histamine, Th2 inflammatory response, and intestinal damage. Oral administration of fucoidan markedly alleviated allergic symptoms by inhibiting mast cell activation and modulating intestinal immune responses. Furthermore, fucoidan significantly ameliorated intestinal immunological dysregulation, maintained barrier integrity, modulated gut microbiota composition, and enhanced short-chain fatty acid (SCFA) production. Mechanistically, the protective effects of fucoidan were closely associated with activation of the AMPK/SIRT1/FOXO1 pathway, which correlated with improved intestinal barrier function. Collectively, these results demonstrate that fucoidan may protect against food allergy by enhancing intestinal barrier function, highlighting the potential of natural biological substances in addressing food allergy.

Alcoholic liver fibrosis (ALF) is a severe hepatic disorder caused by chronic excessive alcohol consumption, involving hepatic stellate cells (HSCs) activation. Fucoidan oligosaccharides (FOS) are marine algae-derived oligosaccharides with diverse biological activities. This study investigated FOS's protective effects against ALF and its molecular mechanisms through in vivo and in vitro experiments. The results indicated that FOS ameliorated liver function injury in mice. FOS reduced serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) while increasing the levels of alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH). FOS alleviated hepatic steatosis and inflammation, and reduced hepatic lipid accumulation and blood lipid levels. Moreover, FOS inhibited the activation of hepatic stellate cells (HSCs), downregulated the expression of α-smooth muscle actin (α-SMA), Collagen - I, and Collagen - III. Bioinformatic analysis integrating five databases with Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses revealed that Signal Transducer and Activator of Transcription-3 (STAT3) is the upstream regulatory gene of fucosyltransferase 8 (FUT8) and closely associates with the Janus Kinase (JAK)/STAT signaling pathway. Molecular docking results indicated that FOS could bind to JAK1 (binding energy = -5.4 kcal/mol). Further experimental studies demonstrated that FOS downregulated the expression of FUT8 and the core fucosylation of TGF-β type I receptor (ALK5) by inhibiting the JAK/STAT3 signaling pathway, thereby suppressing the activity of the TGF-β/Smad signaling pathway. These results demonstrate that FOS, as a natural marine algae-derived functional oligosaccharide, exhibits potential to ameliorate ALF through suppression of the JAK/STAT3/FUT8 axis.

This study investigated the protective properties of fecal microbiota derived from mice treated with sodium alginate (SA) and normal mice with both types immunosuppressed by exposure to antibiotics and cyclophosphamide. A dietary intervention using SA obviously increased the diversity and improved the composition of gut microbiota in normal mice. Fecal microbiota transfer (FMT) from both mice treated with sodium alginate and normal mice alleviated spleen tissue damage and improved immune function. FMT alleviated intestinal mucosal injury and reduced intestinal permeability via increasing mucin and tight junction protein expression. In addition, FMT reduced gut inflammation via down-regulating the expression of toll-like receptor 4 protein. Furthermore, FMT treatment improved the disordered gut microbiota via increasing the abundance of Lactobacillus and Lachnospiraceae NK4A136 group whilst decreasing the abundance of Bacteroides. PICRUSt2 function prediction analysis showed that, compared with the model group, FMT treatment significantly down-regulated lipopolysaccharide biosynthesis and the mitogen-activated protein kinase signaling pathway-fly. Collectively, we found that SA can regulate the gut microbiota structure of normal mice and confirms the effectiveness of FMT in alleviating intestinal barrier damage and gut dysbiosis in antibiotic-cyclophosphamide-induced immunosuppressed mice. This work also reveals that SA can potentially alleviate the immunosuppression caused by cyclophosphamide in mice by modulating the intestinal microbiota and exploiting their functional properties.

Fucoidan is a native sulfated polysaccharide mainly isolated from brown seaweed, with diverse pharmacological activities, such as anti-inflammatory and antifibrosis. Hyperuricemia (HUA) is a common metabolic disease worldwide and mainly causes hyperuricemic nephropathy, including chronic kidney disease and end-stage renal fibrosis. The present study investigated the protective function of fucoidan in renal fibrosis and its pharmacological mechanism. The renal fibrotic model was established with the administration of potassium oxonate for 10 weeks. The protein levels of related factors were assessed in HUA mice by an enzyme-linked immunosorbent assay (ELISA) and western blotting. The results showed that fucoidan significantly reduced the levels of serum uric acid, blood urea nitrogen (BUN), α-smooth muscle actin (α-SMA), and collagen I, and improved kidney pathological changes. Furthermore, renal fibrosis had been remarkably elevated through the inhibition of the epithelial-to-mesenchymal transition (EMT) progression after fucoidan intervention, suppressing the Janus kinase 2 (JAK2) signal transducer and activator of transcription protein 3 (STAT3) signaling pathway activation. Together, this study provides experimental evidence that fucoidan may protect against hyperuricemia-induced renal fibrosis via downregulation of the JAK2/STAT3 signaling pathway.

[Objective]To summarize and discuss the regulatory effects of fucoidan on different components of immune system.[Method]By referring to the literature at home and abroad,this paper summarized and refined the research content of the immunomodula-tory effect of the fucoidan.[Result]Fucoidan is a kind of polysaccharide containing fucose and sulfuric acid groups.It has a variety of biological functions and can enhance the activity of immune organs,non-specific immune system and specific immune system.[Conclu-sion]Fucoidan can improve the immune activity of human body by regulating the function of immune system.

目的:探究褐藻膳食纤维对糖脂代谢的调节作用和防治代谢性疾病的关系。方法:以褐藻膳食纤维、糖脂代谢、肠道菌群、慢性代谢性疾病为检索词在中国知网、万方数据库、维普数据库、PubMed和Web of Science等数据库查找相关文献进行归纳整理。结果:褐藻膳食纤维通过减少糖脂摄入量,抑制糖脂的吸收,促进糖脂排泄等影响机体的糖脂消化吸收能力,调节肠道菌群的种类和数量以及影响肠道菌群代谢产物,从而改善糖脂代谢紊乱,预防其诱导的慢性代谢性疾病。结论:褐藻膳食纤维对调节糖脂代谢和肠道菌群具有重要作用,本文为褐藻膳食纤维在调整机体代谢和防治代谢性疾病方面的开发应用提供了参考。

Obesity is a risk factor for many diseases. Energy intake plays an important role in the development of obesity. Studies have shown that increasing the amount of dietary fiber in diet can boost gut motility, increase satiety, and reduce energy intake. Alginate is a marine fiber extracted from the cell wall of alga. Recently, researchers have paid much attention to the role and mechanism of alginate in controlling dietary energy. In the study, mechanisms and influencing factors for dietary fiber from algae in regulation on energy production, storage and consumption were reviewed.

肥胖症是引起很多疾病的危险因素.随着生活水平的提高,膳食纤维干预与肠道菌群的调节在预防治疗肥胖的作用备受关注.本文对褐藻膳食纤维改善肥胖相关指标,重塑肠道菌群,从而预防肥胖的发生机制予以综述.

This study was aimed to explore the effects of fucoidan on iron overload and ferroptosis-induced liver injury, and the underlying mechanisms in rats exposed to alcohol. Sprague-Dawley rats were used to establish alcoholic liver injury model by intragastric administration with alcohol for 16 weeks. The results showed that fucoidan treatment reversed alcohol-induced increases in reactive oxygen species and malondialdehyde levels, and increased glutathione peroxidase and glutathione levels, thus protecting against liver damage. Long-term alcohol feeding resulted in abnormal increase of serum ferritin, liver total iron and the "free" iron levels. Fucoidan treatment reduced serum ferritin level and alleviated liver iron deposition. Fucoidan reversed the reduction of hepcidin induced by alcohol exposure and decreased divalent metal transporter 1 (DMT1) and ferroportin1 (FPN1) expressions in the duodenum. Electron microscope observation of liver tissues showed that alcohol exposure induced ferroptosis changes in the liver. However, fucoidan treatment could alleviate alcohol-induced ferroptosis via upregulating the expressions of p62, Nrf2, SLC7A11 and GPX4. The liver endogenous metabolites analysis by liquid chromatography and mass spectrometry showed that after fucoidan intervention, mineral absorption, biosynthesis of amino acids pathways and lipid metabolism were changed. Fucoidan intervention reduced the levels of oxidized glutathione and regulated the levels of phosphatidylethanolamines in liver tissues. Our data showed that fucoidan supplementation could inhibit iron load via regulating hepcidin-intestinal DMT1/FPN1 axis, alleviate the liver oxidative damage and protect hepatocytes from ferroptosis induced by long-term alcohol exposure through upregulating p62/Nrf2/SLC7A11 pathway in rats.

目的 探讨褐藻胶对Wilson病(WD)小鼠基底节豆状核变性的神经保护作用和机制.方法 应用铜负荷饮食法建立WD模型,治疗组小鼠每天给予褐藻胶灌胃,对照组同步灌胃等体积的生理盐水,每日1次,连续28 d.电感耦合等离子体质谱法检测尿铜水平,血液分析仪计数血常规指标,生化分析仪检测肝肾功指标(ALT、AST、Urea、Crea),甲苯胺蓝染色法观察豆状核神经细胞的病理变化,原位缺口末端标记法(TUNEL)检测细胞凋亡,免疫组化法检测核转录因子-κB(NF-κB)和基质金属蛋白酶-9(MMP-9)的表达.结果 经褐藻胶干预后,高剂量组小鼠行为功能较模型组显著改善,尿铜水平较模型组显著降低(P＜0.05),血清ALT、AST活性较模型组均显著下降(P＜0.05),变性细胞指数和凋亡细胞指数较模型组均显著降低(P＜0.05),NF-κB和MMP-9表达水平较模型组均显著减弱(P＜0.05).结论 褐藻胶可能通过促进铜离子的排泄,抑制铜离子引起的氧化应激和炎症反应,对基底节豆状核神经细胞发挥保护作用.

目的 探究海藻来源岩藻多糖与代谢性疾病的关系及对肠道菌群的调节作用.方法 以岩藻多糖、慢性代谢性疾病、肠道菌群为检索词在中国知网,万方数据库,维普数据库,PubMed和Web of Science数据库上查找相关文献,并对相关文献进行归纳整理与总结.结果 岩藻多糖具有抗炎、抗氧化、调节代谢、抗菌和抗凝血等多种健康功效在代谢性疾病的发生发展中发挥着重要的作用,肠道菌群可影响机体能量摄取,调节机体的营养代谢.岩藻多糖可调节代谢性疾病的肠道菌群,改善肠道菌群平衡,进而调节糖脂平衡,改善肠道炎症.结论 岩藻多糖在慢性代谢性疾病及肠道菌群的调节中发挥着重要的作用,为预防慢性代谢性疾病的发生,减少手术治疗产生的不良反应,为海藻源性岩藻多糖在调整机体代谢方面的开发应用提供相应参考.

This study investigated the protective effects of sodium alginate (SA) on the gut microbiota, immunity, and intestinal mucosal barrier function in cyclophosphamide-induced immunosuppressed BALB/c mice. SA alleviated spleen tissue damage and restored impaired immune functions, such as increasing the immune organ index, decreasing splenic T lymphocytes, and markedly increasing the secretion of serum immunoglobulins and cytokines in immunosuppressed mice. In addition, SA reversed the intestinal mucosal injury and increased the intestinal permeability by upregulating the expression of tight junction proteins. Moreover, SA decreased gut inflammation by reducing serum d-lactic acid (D-LA) and lipopolysaccharide (LPS) concentrations and downregulating toll-like receptor 4 (Tlr4) and mitogen-activated protein kinase (Mapk) pathway expression. Furthermore, SA significantly increased the abundance of beneficial bacteria (Lactobacillus, Roseburia, and Lachnospiraceae NK4A136) and decreased pathogenic bacteria (Helicobacter, Peptococcus, and Tyzzerella) in the intestine as determined by 16S rRNA gene high-throughput sequencing. In conclusion, our study provides a scientific basis for SA as a functional food in modulating gut microbiota and protecting against intestinal mucosal injury and indicates that SA has potential application for enhancing immunity.

The aim of the study was to detect the neuroprotective activity of fucoidan in alcohol exposure and withdrawal mice and the underlying mechanisms. C57BL/6J mice were used to establish the murine model of chronic alcoholism and withdrawal over 10 weeks of alcohol exposure. After fucoidan treatment, the depression-like behaviors in mice with alcoholism were improved, and 5-hydroxytryptamine and brain derived neurotrophic factor levels were increased both in serum and brain tissues. Fucoidan treatment attenuated the increase of lipopolysaccharide induced by alcohol, and decreased tumor necrosis factor-α and interleukin-1β levels. In hippocampus fucoidan inhibited microglia cell activation, and down-regulated the levels of Toll-like receptor 4 and its downstream protein factors. In addition, fucoidan regulated the structure of gut flora and made the composition of microbiota more similar to that of the normal control mice with increased abundances of Prevotella and Alloprevotella. Oral administration of fucoidan could alleviate the depression-like behaviors of mice with alcoholism through the gut-microbiota-brain axis.

BACKGROUND AND OBJECTIVES:Animal experiments showed that resistant starch (RS) had an antioxidant and antiinflammatory effect. However, clinical studies showed both insignificant and significant effects of RS on inflammation and oxidative stress. The purpose of this work is to conduct a systematic review and meta-analysis of previous randomized controlled trials (RCTs) to investigate these effects.METHODS AND STUDY DESIGN:A systematic literature search was conducted on Web of Science, Scopus, PubMed and Cochrane electronic databases, which included studies from the earliest date of the database to September 2021. Key inclusion criteria were: RCTs; reporting at least one inflammatory or oxidative stress biomarker as endpoint; more than seven day intervention. Key exclusion criteria were: using a mixture of RS and other functional food ingredients as intervention substance; inappropriate controls.RESULTS:A total of 16 RCTs including 706 subjects were included. RS supplementation significantly improved total antioxidant capacity [standard mean difference (SMD) (95% CI): 2.64 (0.34, 4.94), p=0.03], and significantly reduced blood malondialdehyde concentration [SMD (95% CI): -0.55 (- 0.94, -0.17), p=0.01]. RS supplementation significantly reduced blood C-reactive protein concentration in type 2 diabetes mellitus (T2DM) patients [SMD (95% CI): -0.35 (-0.65, -0.05), p=0.02]. RS consumption significantly reduced blood interlukin-6 and tumor necrosis factor- concentration if removing one distinct trial.CONCLUSIONS:RS supplementation may significantly reduce a few oxidative-stress and inflammation biomarkers such as malondialdehyde and C-reactive protein, particularly in T2DM patients. Future work should investigate the optimal dosage of RS supplementation for modulating oxidative stress and inflammation biomarkers related to T2DM.

For alcoholic liver disease (ALD), mitophagy has been reported as a promising therapeutic strategy to alleviate the hepatic lesion elicited by ethanol. This study was conducted to investigate the regulatory effects of fucoidan on mitophagy induced by chronic ethanol administration in rats. Here, 20 male rats in each group were treated with fucoidan (150 and 300 mg per kg body weight) by gavage once daily. Up to 56% liquor (7 to 9 mL per kg body weight) was orally administered 1 h after the fucoidan treatment for 20 weeks. The results showed that chronic ethanol consumption elevated the levels of hepatic enzymes (ALT, AST, and GGT) and triglyceride (TG) contents, with liver antioxidant enzymes being decreased and lipid peroxidation products increased and thus initiating the mitochondria-induced endogenous apoptotic pathway. Furthermore, ethanol-induced excessive oxidative stress inhibited the function of mitochondria and promoted damaged mitochondria accumulation which stimulated the PTEN-induced putative kinase 1 (PINK1) and Parkin associated mitophagic pathway in the liver. In contrast, the fucoidan pretreatment alleviated ethanol-induced histopathological changes, disorders of lipid metabolism, and oxidative damage with mitophagy related proteins and mitochondrial dynamics-related proteins namely mitochondrial E3 ubiquitin ligase 1 (Mul1), mitofusin2 (Mfn2) and dynamin-related protein 1 (Drp1) being restored to a normal level. In summary, our findings suggest that fucoidan pretreatment protects against ethanol-induced damaged mitochondria accumulation and over-activated mitophagy, which plays a pivotal role in maintaining mitochondrial homeostasis and ensuring mitochondrial quality.

褐藻膳食纤维(海藻酸盐,Alg)是存在于海洋食用藻类中的一种酸性多糖,具有多种生物活性作用.研究表明,褐藻膳食纤维可有效地改善肠道菌群的组成结构,通过菌群代谢膳食纤维发酵产物调节宿主机体的代谢水平,从而改善肥胖、糖尿病等代谢相关性疾病.从作为食品添加剂的角度出发,对褐藻膳食纤维作用于人和动物模型体重、血糖、脂代谢以及肠道菌群的效果加以综述,并探讨其潜在机制,为海洋功能性产品的开发和应用提供科学依据.

肠道不仅是人体消化吸收的重要器官,也是维持机体内环境稳态的先天屏障,肠道屏障受损与多种疾病发生发展密切相关.岩藻多糖作为食源性天然产物,具有多种生物学活性.近年来研究发现岩藻多糖通过修复肠黏膜、增强免疫功能、调节肠道菌群等来维护肠道健康.本文主要针对岩藻多糖保护肠道屏障的作用和机制进行综述.

对植物多糖与肠道菌群相关性的研究进展进行综述,为植物多糖的研究与利用提供科学依据.

The intestinal tract is one of the main organs responsible for digestion and absorption, and it also functions as a congenital barrier to maintain the homeostasis of the internal environment of the body. Damage to the intestinal mucosal barrier is closely related to the occurrence and development of a variety of diseases. As a natural food product, fucoidan has a number of biological activities. In recent years, it has been found that it exerts certain protective effects on intestinal physical, chemical, immune and microbial barriers. In the present review article, the role and mechanisms of action of fucoidan in protecting the intestinal mucosal barrier from damage are summarized and discussed. It is hoped that the information presented herein, may shed light onto the functions of fucoidan and may aid its use as a protective strategy against intestinal mucosal barrier dysfunction.

幽门螺杆菌(Hp)是常见的慢性感染致病菌之一,其感染是引起某些临床疾病的危险因素.口腔是除胃以外Hp的另一个储存场所,口腔Hp和胃内Hp具有一定的同源性,而且影响胃内Hp的根除率.本文对口腔Hp和胃Hp相关性研究进展作一综述.