JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
·
2017
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IF 3.154
Yang Li,Ying Peng,Mengyue Wang,Pengfei Tu,Xiaobo Li
Cistanches Herba is taken orally as a health food supplement and medicinal plant in Asian countries. It consists of the stems of Cistanche deserticola (CD) and Cistanche tubulosa (CT). The gastrointestinal metabolism of the multiple components contained in Cistanches Herba is crucial for the discovery of bioactive constituents. This study aims to elucidate the comprehensive metabolic profile of the Cistanches Herba water extract by simulating human gastrointestinal metabolism in vitro independently and sequentially using four models: gastric juice, intestinal juice, human intestinal bacteria, and human intestinal microsomes. A total of 35 and 18 metabolites were characterized from CD and CT water extracts, respectively. These metabolites were formed through reduction, methylation, dimethylation, deglycosylation, decaffeoyl, derhamnose, dehydrogenation, and glucuronidation. The difference in metabolites of the Cistanches Herba water extract and single compounds and the difference in metabolites of CD and CT water extracts were caused by the oligosaccharides and polysaccharides in Cistanches Herba.
研究领域:
药理学
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代谢
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传统医学
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产品关联
DOI
PubMed
高影响因子
Acta Pharmaceutica Sinica B
·
2025
·
IF 14.6
Yuhong Wang,Lin Hu,Lei Wang,Chonghai Zhang,Wenhao Shen,Hongli Yang,Min Li,Xin Zhang,Mengmeng Xu,Muxing Zhang,Kai Yang,Xiaopeng Tian
Inflammatory bowel disease (IBD) is an autoimmune disorder involving complex immune regulation, where balancing localized and systemic immunosuppression is a key challenge. This study aimed to enhance the therapeutic efficacy by engineering the probiotic Escherichia coli Nissle 1917 (EcN). We removed endogenous plasmids pMUT1 and pMUT2 from wild-type EcN and expressed the mPD-L1 (19‒238 aa)-mFc fusion protein on the bacterial surface using a cytolysin A (ClyA) fragment. This modification stabilized mPD-L1 (19‒238 aa) protein expression and promoted its recruitment to outer membrane vesicles (OMVs). The engineered strain, EcNΔ pMUT1/2 -ClyA-mPD-L1-mFc (EcN-ePD-L1-mFc), features conditional ePD-L1-mFc expression under the araBAD promoter, enhancing gut-targeted release and reducing systemic side effects. This strain improved treatment targeting and efficiency by enabling direct ePD-L1-mFc interaction with immune cells at inflammation sites. OMVs from this strain induced Treg proliferation, inhibited effector T cell proliferation in vitro , and significantly improved intestinal inflammation and colonic epithelial barrier repair in vivo . Additionally, the bacterium restored intestinal microbiota balance, increasing Lactobacillaceae and reducing Bacteroides . This study highlights the engineered bacterium's potential for targeted intestinal immune modulation and offers a novel local IBD treatment approach with promising clinical prospects.
研究领域:
微生物学
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免疫学
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分子生物学
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胃肠病学
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合成生物学
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产品关联
DOI
PubMed
高影响因子
Food Bioscience
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2025
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IF 5.9
Kai-Xin Jiang,Jin-Lei Geng,Qin Yuan,Jie Li,Wen Liu,Hong-Yan Liu,Yi-Chen Hu,Liang Zou,Shengpeng Wang,Ding-Tao Wu
Thinned unripe kiwifruit, a significant byproduct of commercial kiwifruit production, contains abundant pectic polysaccharides comparable to mature kiwifruit. Although acidic heteropolysaccharides from mature kiwifruit exhibit potent anti-inflammatory activity, the protective effects of unripe kiwifruit-derived pectic polysaccharides against ulcerative colitis (UC) remain unclear, ultimately limiting their potential utilizations. Therefore, to bridge this knowledge gap and facilitate their utilization, the chemical structures and anti-UC effects of two pectic polysaccharides, TKP (from unripe kiwifruit) and MKP (from mature kiwifruit), were systematically studied and compared. Results demonstrated that TKP and MKP share nearly identical primary chemical structures, predominantly comprising homogalacturonan (HG) and rhamnogalacturonan I (RG-I) domains. Particularly, TKP exhibited a longer side chain length (14.37 vs. 8.21) and higher RG-I content (73.62 mol% vs. 50.02 mol%) than MKP. Furthermore, both TKP and MKP significantly alleviated dextran sulfate sodium (DSS)-induced UC in mice. Notably, TKP exhibited superior effects to MKP in several aspects, such as enhanced butyrate production, more effective restoration of goblet cell populations, enhanced upregulation of tight junction protein ZO-1, and greater reduction in pro-inflammatory cytokines (IL-1β, IL-6, and TNF-α). Both TKP and MKP effectively suppressed pathogenic bacteria (e.g., Escherichia-Shigella and Oscillibacter ) while promoted beneficial bacteria (e.g., Akkermansia and Bacteroides ). Notably, TKP significantly and selectively enhanced Paraprevotella growth, an effect not observed within MKP. These differential effects between TKP and MKP may be linked to their structural differences. Collectively, these findings provide valuable insights to develop TKP as a promising functional food or ingredient for preventing and ameliorating intestinal inflammatory disorders.
研究领域:
食品科学
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胃肠病学
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微生物学
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营养学
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植物学
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药理学
✓ 已验证
产品关联
DOI
高影响因子
PHYTOMEDICINE
·
2024
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IF 6.7
Wang Yi,Jiang Yu,Li Mingxing,Xiao Yaqin,Zhao Qianyun,Zeng Jiuping,Wei Shulin,Chen Shuhan,Zhao Yueshui,Du Fukuan,Chen Yu,Deng Shuai,Shen Jing,Li Xiaobing,Li Wanping,Wang Fang,Sun Yuhong,Gu Li,Xiao Zhangang,Wang Shengpeng,Wu Xu
Background Rosavin (RSV) is a naturally occurring compound isolated from Rhodiola species. While RSV has been reported with pharmacological activities of anti-oxidation, anti-inflammation, anti-stress and immunomodulation, its effect on colitis and the underlying mechanisms remain unclear. Purpose This study aims to investigate whether and how RSV alleviated colitis in mice. Study design and methods The protective effect of RSV (50, 100, 200 mg/kg, p.o.) was investigated in dextran sulfate sodium (DSS) mediated mouse models of acute and chronic colitis. Alterations in fecal microbiota were evaluated by 16S rRNA sequencing. Pseudo germ-free mice achieved by antibiotics treatment were applied to assess the RSV-mediated functional role of gut microbiota in colitis. RNA sequencing was performed to determine RSV-induced colonic response. Primary T cell culture was conducted to examine the effect of RSV on Th17 and Treg differentiation. Whole blood assay, dual luciferase reporter assay, and molecular docking methods were applied to investigate the mechanisms and targets of RSV in Th17 regulation. Results Oral RSV significantly relieved DSS-mediated acute and chronic colitis in mice, which recovered body weight loss, reduced disease activity index, alleviated colon injury, inhibited inflammation, suppressed the apoptosis of intestinal epithelia, and maintained intestinal barrier function. Moreover, RSV specifically regulated intestinal microbiota by recovering DSS-mediated microbial changes and elevating beneficial microbes such as Lactobacillus and Akkermansia . Antibiotics treatment experiment showed that the protective role of RSV was at least partially dependent on gut microbiota; however, in vitro incubation showed that RSV did not directly promote the growth of Lactobacillus and Akkermansia strains. Further analysis showed that RSV-mediated genetic alterations in colon were enriched in pathways related to lymphocyte regulation. Additionally, RSV regulated the balance of Th17/Treg in colitis mice. Importantly, RSV inhibited the differentiation of Th17 cell in vitro , suppressed the production of IL-17 by Th17 cells, and downregulated Rorc encoding RORγt and its downstream Il17 . RSV significantly inhibited the RORγt transcription activity and bound to its ligand binding domain. Conclusion RSV alleviates murine colitis through regulating intestinal immunity. Notably, RSV is identified as a novel regulator of Th17 cells that inhibits RORγt-mediated Th17 differentiation. These findings potentiate the Rhodiola -derived natural chemicals as novel anti-colitis agents.
研究领域:
药理学
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免疫学
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微生物学
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分子生物学
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DOI
高影响因子
INTERNATIONAL IMMUNOPHARMACOLOGY
·
2024
·
IF 4.8
Fang Shi,Yong-Sheng Gao,Shu-Mei Han,Cheng-Suo Huang,Qing-Sheng Hou,Xiao-wen Wen,Ben-Shi Wang,Zhen-Yu Zhu,Lei Zou
Metabolic changes have been linked to the development of inflammatory bowel disease (IBD), which includes colitis. Allulose, an endogenous bioactive monosaccharide, is vital to the synthesis of numerous compounds and metabolic processes within living organisms. Nevertheless, the precise biochemical mechanism by which allulose inhibits colitis remains unknown. Allulose is an essential and intrinsic protector of the intestinal mucosal barrier, as it maintains the integrity of tight junctions in the intestines, according to the current research. It is also important to know that there is a link between the severity of inflammatory bowel disease (IBD) and colorectal cancer (CRC), chemically-induced colitis in rodents, and lower levels of allulose in the blood. Mice with colitis, either caused by dextran sodium sulphate (DSS) or naturally occurring colitis in IL-10 -/- mice, had less damage to their intestinal mucosa after being given allulose. Giving allulose to a colitis model starts a chain of reactions because it stops cathepsin B from ejecting and helps lysosomes stick together. This system effectively stops the activity of myosin light chain kinase (MLCK) when intestinal epithelial damage happens. This stops the breakdown of tight junction integrity and the start of mitochondrial dysfunction. To summarise, the study's findings have presented data that supports the advantageous impact of allulose in reducing the advancement of colitis. Its ability to stop the disruption of the intestinal barrier enables this. Therefore, allulose has potential as a medicinal supplement for treating colitis.
研究领域:
胃肠病学
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药理学
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分子生物学
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产品关联
DOI
PubMed
高影响因子
ACS Nano
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2025
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IF 16
Yaoyu Hu,Pengfei Zhu,Junwei Deng,Yi Yu,Qian Chen,Haitao Wu,Zhengbao Zha,Hua Wang,Yan Ma
Individuals diagnosed with inflammatory bowel disease (IBD) frequently encounter dysbiosis of the intestinal microbiota and are predisposed to psychiatric comorbidities, such as depression and anxiety. The development of oral therapeutics that concurrently attenuate intestinal inflammation, modulate gut microbiota, and ameliorate psychiatric symptoms is imperative for effective IBD management. This study introduced an orally administered Inulin gel incorporating magnesium diboride nanosheets (MgB2@Inulin gel). The hydrolysis of MgB2 nanosheets could generate reductive hydrogen gas (H2), which is critical for scavenging excess reactive oxygen/nitrogen species (RONS), and boron ions that neutralize harmful lipopolysaccharides (LPS). Prebiotic Inulin could effectively protect MgB2 nanosheets from gastric acid degradation, ensuring their persistence in the intestinal tract, where it modulated the gut microbiota and preserved intestinal barrier integrity. Notably, MgB2@Inulin gel markedly alleviated anxiety and depressive behaviors in the model of colitis by regulating the gut–brain axis. Thus, this work underscores the pivotal role of the gut–brain axis in the therapeutic approach to IBD and its associated psychiatric manifestations, proposing a straightforward, safe, and efficacious oral hydrogen treatment strategy for IBD and concurrent mental health disorders.
研究领域:
纳米医学
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胃肠病学
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神经科学
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微生物学
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药理学
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材料科学
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免疫学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
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2024
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IF 7.7
Minghui Wang,Xiaoxuan Xu,Mingxuan Sheng,Ming Zhang,Fang Wu,Zhi Zhao,Meng Guo,Bing Fang,Jianmin Wu
Tannic acid, a bioactive polyphenol found in various phytogenic foods and medicinal plants, has potential prevention effects on colitis, though more evidence and mechanistic studies are required to substantiate this. In this study, we investigated the effects of different doses from 0 to 3 mg/mL of tannic acid on mice, ultimately selecting a dose of 3 mg/mL for the anti-colitis trial based on growth and intestinal morphology assessments. Using the DSS-induced colitis model, we found that tannic acid may alleviate colitis by inhibiting the IL-17 - NF-κB p65 signaling pathway and modulating epigenetic pathways, particularly methylation modifications. Additionally, tannic acid altered the gut microbiota, increasing the abundances of Prevotella , Eubacterium_siraeum_group , and Enterorhabdus in the colon. Supplementation with Eubacterium siraeum via gavage also inhibited colitis, accompanied by increased folate and methylation regulators in the colon. These findings suggest that tannic acid may inhibit colitis through the suppression of the IL-17 - NF-κB pathway and the enhancement of microbiota-mediated methylation pathways.
研究领域:
免疫学
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胃肠病学
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微生物学
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分子生物学
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药理学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
PHYTOMEDICINE
·
2023
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IF 7.9
Yuanyuan Wei,Yimeng Fan,Sijuan Huang,Jianyu Lv,Yannan Zhang,Zhihui Hao
Background Diarrhea-predominant irritable bowel syndrome (IBS-D) is a common functional gastrointestinal disease. Besides, baizhu shaoyao decoction (BSD) is an effective treatment for IBS-D; however, its mechanism of action remains unclear. Purpose This study aims to assess the ability of BSD to therapy IBS-D and to elucidate the underlying mechanism. Methods First, comprehensive analyses, including ADME (absorption, distribution, metabolism, excretion) screening, Venn analysis, Gene Ontology (GO) analysis, and network construction, were performed to characterize IBS-D-related pathways and explore the synergistic effects of BSD active compounds. Next, an IBS-D model was constructed using a three-factor superposition method of neonatal maternal separation, chronic immobilization stress stimulation, and Sennae folium aqueous extract lavage. Moreover, the impact of BSD was assessed based on the body weight, fecal water content, and abdominal withdrawal reflex (AWR), and the results of the open field test, sucrose preference test, intestinal permeability assessment, transmission electron microscopy, and TdT-mediated dUTP nick-end labeling (TUNEL) analysis. The factors that regulate the BSD effects on IBS-D were estimated using immunoblotting, quantitative reverse transcription polymerase chain reaction (q-RTPCR), immunohistochemistry, and transcriptome sequencing analyses. Results We found that BSD improved depressive behavior, brain–gut peptide levels, and intestinal permeability induced by IBS-D by increasing the abundance of intestinal tight junctions. In addition, BSD reduced secretory immunoglobulin A levels and the number of intestinal mast cells in IBS-D rats. Network pharmacology and transcriptome sequencing analysis further revealed that the forkhead box O (FoxO) signaling pathway contributed to the BSD-induced alleviation of IBS-D, as BSD regulated the protein and mRNA levels of FoxO1, glycogen synthase kinase 3β, and FoxO3a. Importantly, a FoxO1 inhibitor effectively alleviated IBS-D symptoms in rats, whereas a FoxO3a agonist had the opposite effects. Conclusion These results demonstrate that BSD alleviates depression and intestinal symptoms by regulating brain–gut peptide expression and restoring the intestinal barrier function via the FoxO signaling pathway. Furthermore, our study uses serum pharmacochemistry technology to analyze the in vivo components of TCM formula under effective condition, solving the problem of the discovery of the effective components of TCM to some extent.
研究领域:
药理学
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胃肠病学
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神经科学
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分子生物学
✓ 已验证
DOI
PubMed
高影响因子
PLoS Neglected Tropical Diseases
·
2024
·Vol. 18
·期 12
·e0012714
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IF 3.4
Xuanyin Cui,Yi Cheng,Hongyan Wang,Xiaomao Li,Jinfu Li,Ke Zhang,Rong Mou
Ulcerative colitis (UC) is a chronic inflammatory bowel disease with an unknown etiology and is difficult to treat. Studies have shown that some helminths and their associated products have therapeutic potential in controlling or preventing inflammatory diseases. This study is to investigate the mitigation effects of Hymenolepis nana antigens (HnAg) on the UC model. HnAg significantly improved the disease activity index, colon length, and colonic pathological damage in mice with dextran sulfate sodium (DSS)-induced colitis. HnAg intervention could protect the number of goblet cells and enhance the expression of tight junction proteins and mucins, thereby improving intestinal barrier integrity. HnAg attenuated small intestinal organoid damage and stimulated intestinal stem cells proliferation in a DSS-induced mouse organoid inflammation model. The protective mechanism of HnAg might be related to the activation of the aryl hydrocarbon receptor (AhR)/IL-22 signaling pathway, which regulates intestinal barrier function and promotes the proliferation and differentiation of intestinal stem cells. In conclusion, HnAg has a therapeutic effect on UC mice. Our study provides a new approach for alleviating UC by Hymenolepis nana and its associated products.
Ulcerative colitis (UC) is an immune-mediated chronic inflammatory disease. Currently, commonly used drugs such as aminosalicylates and glucocorticosteroids are difficult to treat and have many adverse effects. In recent years, there has been a growing interest in utilizing the immunomodulatory abilities of worms to develop new therapies for the treatment of inflammatory and allergic diseases. Hymenolepis nana is a zoonotic parasitic worm that parasitizes the small intestines of humans and rodents and generally does not cause serious pathologic damage to their hosts, making it a potential class of intestinal parasites in helminthic therapy. In this study, we investigated the mitigating effect of Hymenolepis nana antigens (HnAg) on UC in mice from the perspective of maintaining intestinal mucosal barrier integrity. The results showed that HnAg alleviated UC in mice by activating the aryl hydrocarbon receptor (AhR)/IL-22 signaling pathway, promoting the proliferation and differentiation of intestinal stem cells, and modulating the integrity of the intestinal mucosal barrier. Meanwhile, HnAg attenuated DSS-induced inflammatory damage in mouse small intestinal organoid tissues and promoted intestinal stem cells proliferation. Suggesting that Hymenolepis nana and its related products may become a new option for alleviating UC.
研究领域:
免疫学
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胃肠病学
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药理学
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炎症性肠病
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DOI
PubMed
高影响因子
JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
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2024
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IF 5.7
Yaqian Li,Hongtao Xu,Liuyang Zhou,Yuwei Zhang,Wenqing Yu,Shubo Li,Jie Gao
In this study, we aimed to explore the protective effects of Bifidobacterium in colitis mice and the potential mechanisms. Results showed that Bifidobacterium breve (B. breve) effectively colonized the intestinal tract and alleviated colitis symptoms by reducing the disease activity index. Moreover, B. breve mitigated intestinal epithelial cell damage, inhibited the pro-inflammatory factors, and upregulated tight junction (TJ)-proteins. Gut microbiota and metabolome analysis found that B. breve boosted bile acid-regulating genera (such as Bifidobacterium and Clostridium sensu stricto 1), which promoted bile acid deconjugation in the intestine. Notably, cholic acid (CA) was closely associated with the expression levels of inflammatory factors and TJ-proteins (p < 0.05). Our in vitro cell experiments further confirmed that CA (20.24 ± 4.53 pg/mL) contributed to the inhibition of lipopolysaccharide-induced tumor necrosis factor-α expression (49.32 ± 5.27 pg/mL) and enhanced the expression of TJ-proteins (Occludin and Claudin-1) and MUC2. This study suggested that B. breve could be a probiotic candidate for use in infant foods.
研究领域:
胃肠病学
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微生物学
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免疫学
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营养学
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产品关联
DOI
PubMed
高影响因子
Current Research in Food Science
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2025
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IF 7
Liang Lei,Jing Wang,Juanjuan Wang,Wenjuan He,Tao Wu,Jing Li,Xiaobin Bi,Mei Mei,Xinlei Guan,Xiaoqiang Zhu
Ulcerative colitis (UC) is a severe inflammatory bowel disease marked by intestinal inflammation, compromised barrier function, and gut microbiota imbalance, with a restricted range of therapeutic options currently available. Quercetin, a flavonoid extracted from fruits and vegetables, have been shown significant anti-inflammatory and microbiota-modulating effects. However, the interactions between gut microbes and quercetin in colitis remain insufficiently elucidated. This research delved into the potential involvement of the gut microbiota-isovanillic acid (IVA)-intestinal barrier axis in the anti-colitis effects of quercetin via 16S rDNA sequencing and metabolomics. Quercetin administration effectively enhanced gut barrier integrity and mitigated colitis by boosting IVA production through modulating gut microbiota composition, particularly increasing Clostridium_XIVa and Clostridium_XI abundances. Notably, gut microbiota depletion with antibiotics (ABX) treatment markedly diminished IVA production and concurrently negated quercetin's positive effects on colitis. More importantly, IVA supplementation was also effective in alleviating colitis via enhancing gut barrier function, suggesting gut microbiota-derived IVA supported beneficial effects of quercetin on colitis. Our research highlighted the crucial involvement of gut microbial-derived IVA in the anti-colitis effects of quercetin and underscored its therapeutic potential, along with IVA, as a treatment for colitis and other intestinal inflammatory conditions.
研究领域:
药理学
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微生物学
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免疫学
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营养学
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胃肠病学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
·
2021
·
IF 5.279
Xuejiao Zhang,Jiaxin Gu,Congying Zhao,Yaozhong Hu,Bowei Zhang,Jin Wang,Huan Lv,Xuemeng Ji,Shuo Wang
Non-nutritive sweeteners are the most widely used food additives designed to provide sweetness and reduce caloric intake. Studies have confirmed a link between sweeteners and colitis, yet supporting scientific data remain exiguous and controversial. In this study, three common sweeteners (Saccharin sodium, Stevioside, and Sucralose) in acceptable daily intake dosage were added to water in order to determine their effects on dextran sodium sulfate-induced colitis in mice. Our results show that the three sweeteners meliorate colitis to varying degrees─Saccharin exerts the most pronounced effect, followed by Stevioside and Sucralose. Intake of sweeteners alleviates colitis symptoms, alters gut microbiota, reshapes the TH17/Treg balance, protects the intestinal barrier, and reduces inflammation. Most significantly, sweeteners can enhance the abundance of Mucispirillum and Alistipes, which are conducive to colitis recovery, and upregulate the expression of E-cadherin through the miR-15b/RECK/MMP-9 axis to improve intestinal barrier integrity. Moreover, by inhibiting the MMP-9/AKT/NF-κB pathway, inflammation is relieved, as reflected in the restoration of the Th17/Treg balance. Our results link the consumption of sweeteners to the remission of colitis, which provides new scientific evidence for the safe use of sweeteners.
研究领域:
药理学
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免疫学
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胃肠病学
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微生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
危险品化学品经营许可证（带存储）