BIOORGANIC CHEMISTRY
·
2026
·
IF 5.1
Qian Zhang,Wenyu Wang,Chenhan Wu,Qingting Du,Weili Yin,Jiaheng Chen,Jian Ma,Chong Li,Shaojie Zhang
Ulcerative colitis (UC) is characterized by recurrent inflammation of the gastrointestinal tract, and currently available treatment drugs are limited. Plant-derived polysaccharides hold promise for UC prevention. A water-soluble α -D-glucan (CLP80–1) with a molecular weight of 8.17 × 10 5 Da was isolated and characterized from the roots of traditional Chinese medicinal plant Crepis lignea . Structural analysis revealed that its repeating units comprise →6)- α -D-Glc p -(1 → and →3,6)- α -D-Glc p- (1 → residues as the backbone, with α -D-Glc p -(1 → as side chains substituted at C-3. The protective effects of CLP80–1 on dextran sulfate sodium (DSS)-induced ulcerative colitis (UC) in Drosophila melanogaster were investigated. Our results demonstrated that treatment with 1% CLP80–1 significantly improved survival rates, attenuated gut atrophy, reduced intestinal permeability, enhanced intestinal barrier function, suppressed excessive proliferation of intestinal stem cells (ISCs) and enteroblasts (EBs), and inhibited the death of intestinal epithelial cells (IECs). Metabolomic and transcriptomic analyses revealed that CLP80–1 mainly affected amino acid metabolism, TCA cycle, oxidative phosphorylation and JAK/STAT signaling pathway. Furthermore, CLP80–1 reduced reactive oxygen species (ROS) levels, suppressed the expression of pro-inflammatory factors, and downregulated the JAK-STAT signaling pathway, thereby mitigating oxidative stress and inflammatory responses. These findings suggest that CLP80–1 is effective in alleviating intestinal inflammation and may serve as a promising therapeutic candidate for addressing gut inflammatory conditions.
✓ 已验证
产品关联
DOI
PubMed
高影响因子
JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
·
2026
·Vol. 74
·期 30
·23556-23575
·
IF 6.7
Li Wennian,Huang Yujie,Su Hualing,Nong Jiale,Liang Wenyu,Liu Yonghong,Zhao Longyan,Yuan Qingxia
Pectic
polysaccharides hold therapeutic potential for ulcerative
colitis (UC). This study reports the first isolation of two structurally
distinct pectins from Avicennia marina fruit pericarp: AMPP-2-1 (158 kDa), a rhamnogalacturonan-I (RG-I)-rich
pectin with galactan branches and intricate arabinan side chains rich
in β-Ara f terminals; and AMPP-2-2 (16 kDa),
a low-molecular-weight homogalacturonan (HG)-rich pectin with unsaturated
Gal p A at the nonreducing ends. Both pectins significantly
ameliorated dextran sodium sulfate-induced UC by suppressing inflammation,
restoring intestinal barrier integrity, and modulating gut microbiota
to enrich beneficial bacteria while depleting pathogenic bacteria,
alongside promoting short-chain fatty acid production. Low-molecular-weight
HG showed greater ameliorative effects than RG-I under the present
experimental conditions. These findings establish that pectins may
contribute, at least in part, to the intestinal benefits of A. marina fruits in traditional use, expanding the
structural diversity and biomedical applications of pectic polysaccharides
from underexplored plant resources.
✓ 已验证
产品关联
DOI
PubMed
高影响因子
JOURNAL OF ETHNOPHARMACOLOGY
·
2026
·
IF 6.8
Xin Gao,Zhen-Zi Shang,Qiang-Ming Li,Feng-Yun Zhang,Xue-Qiang Zha,Jian-Ping Luo
Ethnopharmacological relevance Dendrobium huoshanense has been long used to treat gastrointestinal disorders including ulcerative colitis (UC) in traditional Chinese medicine. Polysaccharides as its main active components can alleviate UC by reducing inflammation, and promote the secretion of glucagon-like peptide-1 (GLP-1), which possesses anti-inflammatory effects via GLP-1 receptor (GLP-1R). However, it remains unclear whether polysaccharides from different parts of this herb are equally effective in alleviating UC and whether polysaccharides function via GLP-1/GLP-1R axis. Aim of the study To identify the part in which the polysaccharide is most effective in alleviating UC and to explore its mechanism of action through GLP-1/GLP-1R axis. Materials and methods The physicochemical properties of polysaccharides were analyzed. A dextran sulfate sodium (DSS)-induced UC mouse model was used to assess colitis-associated damage via morphological scoring, histopathological evaluation and inflammatory examination with multi-cytokine array and western blotting. Gut microbiota compositions, short-chain fatty acid contents and GLP-1 levels were measured, and their roles were checked using antibiotic mixture and GLP-1R antagonist Exendin (9-39). Results Stem, leaf and flower polysaccharides, with different molecular weight, monosaccharide composition and spatial conformation, differentially alleviated UC symptoms, and stem polysaccharide (DHPS) showed the strongest efficacy, as evidenced by improved epithelial integrity, mucus barrier and inflammatory disorder. DHPS-alleviated UC was independent of DHPS-altered gut microbiota and positively correlated with DHPS-elevated GLP-1 levels, which could be abolished by Exendin (9-39), suggesting that GLP-1-activated GLP-1R signaling mediated the effects of DHPS against UC. Conclusions DHPS is the most effective polysaccharide for alleviating DSS-induced UC through GLP-1/GLP-1R axis, proposing DHPS is a valid candidate for UC treatment using D. huoshanense .
✓ 已验证
DOI
PubMed
高影响因子
Foods
·
2026
·Vol. 15
·期 10
·1675
·
IF 6
Weiyun Zheng,Shugang Li,Yuxin Xu,Shuang Song,Chunqing Ai
Astaxanthin (Ax) is a potent antioxidant, yet its poor water solubility and instability limit its application. While alginate-Ca encapsulation protects Ax during digestion, its release in the colon is often inefficient. This study aims to optimize colon-targeted delivery by integrating inulin and fucoidan, which respond selectively to Bacteroides -mediated fermentation. A novel delivery system was developed using Ax-containing particles formulated in an alginate–inulin–fucoidan matrix (Ax-Mix), with most particles ranging from 2 to 20 μm. In vitro results showed that the incorporation of inulin and fucoidan enhanced Ax release in alginate-Ca (Ax-Alg) through Bacteroides fermentation. Ax-Mix exhibited robust structural integrity under varying pH, thermal, and ionic conditions. Ax-Mix remained intact through the oral cavity, stomach, and small intestine, but disintegrated in the colon, triggering Ax release. Ax-Mix alleviated colitis in mice, characterized by increased weight gain and colon length and reduced disease activity index, tissue damage, and oxidative stress. Ax-Mix reshaped the gut microbiota by increasing microbial diversity and enriching beneficial taxa linked to colitis improvement. These alterations resulted in increased propionate and butyrate production. Compared to Ax-Alg, Ax-Mix exhibited superior therapeutic effects on colitis, though the underlying mechanisms require further investigation. This study presents a promising strategy for microbiota-targeted delivery of active substances.
✓ 已验证
DOI
PubMed
高影响因子
Frontiers in Pharmacology
·
2024
·
IF 4.4
Shu Long,Fu Hangjie,Pi Aiwen,Feng Yuliang,Dong Hui,Si Caijuan,Li Songtao,Zhu Feiye,Zheng Peifen,Zhu Qin
Ulcerative colitis (UC) is a recurring inflammatory bowel disease, in which oxidative stress plays a role in its progression, and regulation of the oxidative/antioxidative balance has been suggested as a potential target for the treatment of UC. The aim of this study was to evaluate the protective effect of andrographolide against UC and its potential antioxidant properties by modulating the nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) pathway. Dextran sulfate sodium (DSS) -induced UC mice and the LPS-induced HT29 inflammatory cell model were established to uncover the potential mechanisms of andrographolide. ML385, a Nrf2 inhibitor, was used in both models to assess whether andrographolide exerts a protective effect against UC through the Nrf2/HO-1 pathway. The in vivo experiment showed that andrographolide ameliorated the symptoms and histopathology of DSS-induced mice and restored the expressions of ZO-1, Occludin-1 and Claudin-1. Meanwhile, DSS-induced oxidative stress and inflammation were suppressed by andrographolide treatment, along with the upregulation of key proteins in the Nrf2/HO-1 pathway. In vitro experiments showed that andrographolide attenuated LPS-induced excessive generation of ROS in HT29 cells, reduced inflammatory factors, and upregulated the expression of proteins related to tight junctions and Nrf2/HO-1 pathway. In addition, ML385 abolished the beneficial effect of andrographolide. In conclusion, the protective effect of andrographolide against UC may involve the suppression of oxidative stress and inflammation via the Nrf2/HO-1 pathway.
研究领域:
药理学
·
炎症性肠病
·
分子生物学
✓ 已验证
DOI
PubMed
高影响因子
Biomaterials Science
·
2019
·Vol. 7
·期 10
·4299-4309
·
IF 5.251
Ya Wu,Minghui Sun,Dan Wang,Genyun Li,Jiangeng Huang,Songwei Tan,Lin Bao,Qian Li,Gao Li,Luqin Si
To effectively alleviate acute severe ulcerative colitis (ASUC), we developed a colon-specific delivery system—PLGA–KPV/MMT/CS multifunctional medicinal nanoparticles loaded with cyclosporine A (CyA). The lysine–proline–valine (KPV) tripeptide, which possesses anti-inflammatory properties and high affinity to peptide transporter 1 (PepT1), can target therapy-related cells (colonic epithelial cells and macrophages) via overexpression of PepT1. Montmorillonite (MMT)/chitosan (CS) coating can reduce CyA leakage in the upper gastrointestinal tract (GIT) and enhance nanoparticle adhesion to the inflamed colon. The bio-distribution demonstrated that nanoparticles can specifically accumulate in the inflamed tissues and can be retained for up to 36 h. After being treated with the CyA–PLGA–KPV/MMT/CS nanoparticles (PKMCN), the mice with DSS-induced ulcerative colitis exhibited significant improvements in body weight, colon length, and disease activity index. Moreover, biochemistry and immunohistochemical analysis showed that the PKMCN treatment group performed as well as the healthy group. Intriguingly, PKMCN without CyA also presented marked therapeutic effects. Our results suggested that PKMCN could be a promising drug delivery system for ASUC therapy by targeting inflamed cells, prolonging curative time, and mitigating colitis.
研究领域:
药学
·
胃肠病学
·
纳米医学
·
炎症性肠病
✓ 已验证
产品关联
DOI
PubMed
高影响因子
BIOCHEMICAL PHARMACOLOGY
·
2025
·
IF 5.6
Xuejun Jiang,Pengcheng Wu,Hui Chen,Jialu Cui,Xiting Lv,Linna Ha,Mingyang Wu,Min Chen,Baojian Wu,Haiman Xu,Dong Dong
Intestinal bowel disease (IBD), prevalent among sleep-deprived populations, is closely associated with circadian rhythm disruptions. Evidence suggests that sleep deprivation (SD) exacerbates colitis; however, the mechanisms is remains poorly understood. We subjected mice with Dextran sulfate sodium (DSS) induced acute and chronic colitis to 6 h-SD per day. It was observed that mild SD significantly aggravated both acute and chronic colitis, involving progressive body weight loss, increased Disease Activity Index (DAI), shortened colon length, histopathological deterioration, and elevated levels of inflammatory cytokines. Circadian gene screening identified PER2 as a pivotal mediator in SD aggravating colitis. Both SD and colitis independently suppressed Per2 expression in mice colon. Notably, the inhibitory effect on PER2 was most pronounced in cases of colitis accompanied by SD. Consistent with this, Per2 deficiency heightened the susceptibility of mice to DSS-induced colitis. Furthermore, transcriptomic analysis revealed that the disordered arachidonic acid (AA) metabolism pathway was implicated in the exacerbation of colitis due to Per2 deficiency. Specifically, Ptgs2 , a gene coding AA metabolism enzyme COX-2, was significantly upregulated in both Per2 -/- colitis mice and SD colitis mice. The elevated PGE 2 levels in plasma and colon supported the involvement of COX-2 mediated proinflammatory conversion of AA during episodes of SD-related colitis aggravation. Mechanistically, in vitro experiments in CT-26 cells suggested Per2 suppressed COX-2 transcription via BMAL1. In summary, SD inhibited the expression of clock factor PER2 in colon, leading to disorder of COX-2-mediated AA metabolism; this process released more pro-inflammatory mediators thereby aggravating colitis
研究领域:
免疫学
·
分子生物学
·
胃肠病学
·
时间生物学
·
炎症研究
✓ 已验证
产品关联
DOI
PubMed
高影响因子
JOURNAL OF CHROMATOGRAPHY A
·
2024
·
IF 3.8
Jiachun Lin,Xue Yang,Anhui Wang,Jinni Yang,Yuan Zheng,Haijuan Dong,Yuan Tian,Zunjian Zhang,Min Wang,Rui Song
Oxysterols and cholesterol precursors are being increasingly investigated in humans and laboratory animals as markers for various diseases in addition to their important functions. However, the quantitative analysis of these bioactive molecules is obstructed by high structural similarity, poor ionization efficiency and low abundance. The current assay methods are still cumbersome to be of practical use, and their applicability in different bio-samples needs to be evaluated and optimized as necessary. In the present work, chromatographic separation conditions were carefully studied to achieve baseline separation of difficult-to-isolate compound pairs. On the other hand, an efficient sample purification method was established for colon tissue samples with good recoveries of sterols, demonstrating negligible autoxidation of cholesterol into oxysterols. The developed UPLC-APCI-MS/MS method was thoroughly validated and applied to measure oxysterols and cholesterol precursors in colon tissue of dextran sulfate sodium (DSS)-induced mouse colitis models, and it is expected to be successfully applied to the quantitative determination of such components in other tissue samples.
研究领域:
分析化学
·
药理学
·
分子生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
PHYTOMEDICINE
·
2021
·
IF 5.34
Yajie Cai,Bing Xu,Fei Zhou,Jianzhi Wu,Shuo Li,Qi Zheng,Yajing Li,Xiaojiaoyang Li,Feng Gao,Shifen Dong,Runping Liu
Background Ulcerative colitis (UC) is a chronic relapsing inflammatory disease that markedly elevates the risk of colon cancers and results in disability. The disrupted immune homeostasis has been recognized as a predominant player in the pathogenesis of UC. However, the overall remission rate of current therapies based on immunoregulation is still unsatisfactory. Si-Ni-San (SNS) has been found effective in relieving UC through thousands of years of clinical practice, yet the specific mechanisms of the protective effect of SNS were not fully elucidated. Purpose We aim to investigate the therapeutic effects of SNS against the development of chronic colitis and the underlying mechanisms. Methods We established a DSS-induced chronic experimental colitis mouse model to evaluate the effect of SNS. RNA-sequencing, bioinformatic analysis, and in vitro studies were performed to investigate the underlying mechanisms. Results Our data demonstrated that SNS significantly ameliorated chronic experimental colitis via inhibiting the expression of genes associated with inflammatory responses. Interestingly, SNS significantly suppressed DSS-induced type I interferon (IFN) responses instead of directly downregulating the production of pro-inflammatory cytokines, such as Il-6. In vitro study further found that SNS selectively inhibited STING and RIG-I pathway-induced type I IFN responses by modulating TBK1- and IRF3-dependent signaling transduction. SNS also suppressed the expression of IFN-stimulated genes by directly inhibiting STAT1 and STAT2 activation. Conclusion Our study not only provides novel insights into the pathogenic role of type I IFN responses in colitis but also suggested that SNS or bioactive compounds derived from SNS may serve as novel therapeutic strategies for the treatment of UC via interfering type I IFN-mediated inflammation.
研究领域:
药理学
·
免疫学
·
胃肠病学
·
分子生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
INTERNATIONAL IMMUNOPHARMACOLOGY
·
2026
·
IF 5.6
Shangping Xing,Xue Cheng,Shiyu Hou,Lidan Qin,Juan Wang,Yue Ding,Zhangyang Shen,Ziteng Dai,Xiaoming Huang,Yanying Liu,Dan Zhu
Novel therapeutic agents with improved safety and efficacy are urgently required for ulcerative colitis (UC), a refractory inflammatory bowel disease. Mangrove-derived natural products represent a promising reservoir for drug discovery. Monomethylsulochrin (MMSC) is a type II polyketide isolated from the endophytic fungus Aspergillus fumigatus of the mangrove plant Aegiceras corniculatum . However, its therapeutic effects on UC and the underlying mechanisms remain unclear. Herein, we evaluated the efficacy of MMSC by using a dextran sodium sulfate (DSS)-induced colitis mouse model and elucidated the underlying mechanisms by proteomics analyses, molecular biology techniques, and 16S rDNA gene sequencing. Our results demonstrated that MMSC significantly ameliorated DSS-induced colitis, as evidenced by reduced disease activity index, preserved colon length, and attenuated histopathological damage. Mechanistically, proteomics profiling and subsequent validation confirmed that MMSC concurrently suppressed the interleukin (IL)-17 and tumor necrosis factor (TNF) signaling pathways by downregulating key nodes (matrix metalloproteinase [MMP]-9, S100 calcium-binding protein A8 [S100a8], CCAAT/enhancer-binding protein beta [Cebpb], cAMP responsive element binding protein 1 [Creb1], and Fas) and related pro-inflammatory cytokines (interleukin [IL]-1β, IL-6, IL-17, TNF-α) in both colonic tissues and lipopolysaccharide (LPS)-stimulated NCM460 cells. Furthermore, MMSC restored gut microbial diversity and composition in mice with colitis, reversing DSS-induced dysbiosis. Spearman correlation analysis revealed that the IL-17/TNF pathway exhibited a notable correlation with MMSC-mediated restoration of the gut microbiota. In conclusion, MMSC alleviates UC through a dual mechanism integrating suppression of IL-17/TNF signaling and restoration of gut microbiota homeostasis, highlighting it as a promising candidate for developing novel therapies against UC.
✓ 已验证
产品关联
DOI
高影响因子
FOOD RESEARCH INTERNATIONAL
·
2026
·
IF 8.8
Xinjiu Deng,Haikun Li,Jiamei Hou,Changci Tong,Jinpeng Liu,Yanwen Zhu,Yunen Liu
• Purified Tremella polysaccharide-rich fraction was physicochemically defined. • • TPS alleviated DSS-induced colitis and preserved barrier-related proteins. • • TPS reduced colonic inflammatory cytokines under DSS-induced injury. • • TPS was associated with partial shifts in DSS-disrupted gut microbiota. • • TLR4/MyD88/NF-κB changes were interpreted as downstream readouts. Tremella fuciformis is a widely consumed edible fungus and a source of structurally diverse polysaccharides, but the intestinal biofunctionality of a purified Tremella polysaccharide-rich fraction remains insufficiently defined. In this study, a purified T. fuciformis polysaccharide-rich fraction (TPS) was obtained by hot-water extraction, ethanol precipitation, anion-exchange chromatography, and gel filtration. TPS was characterized using carbohydrate/protein analysis, gel permeation chromatography (GPC), monosaccharide composition analysis, Fourier-transform infrared spectroscopy (FTIR), X-ray diffraction (XRD), atomic force microscopy (AFM), scanning electron microscopy (SEM), 1 H NMR, dynamic light scattering (DLS), zeta-potential analysis, and thermogravimetric analysis. TPS contained 96.13% total carbohydrate and 5.61% protein and showed features of a mannose-rich acidic heteropolysaccharide, including mainly amorphous organization, aggregated morphology, mixed anomeric proton signals, hydrated colloidal aggregates, negative surface charge, and staged thermal degradation behavior. Its intestinal effects were evaluated in a dextran sulfate sodium (DSS)-induced colitis mouse model. Oral TPS administration alleviated DSS-induced colonic injury, as indicated by improved disease activity and histological features, preservation of ZO-1 and Occludin expression, and reduced colonic TNF-α, IL-1β, and IL-6 levels. TPS was also associated with partial changes in DSS-disrupted gut microbiota profiles and with lower downstream inflammatory protein readouts in the TLR4/MyD88/NF-κB pathway. Molecular docking of TPS-associated monosaccharides was retained only as supplementary exploratory in silico context and was not interpreted as evidence of intact TPS binding, validated receptor engagement, or direct in vivo TLR4 targeting. Overall, this study connects fraction-level compositional and physicochemical characterization of a food-derived Tremella polysaccharide-rich fraction with measurable intestinal barrier-, inflammation-, and microbiota-related responses, providing a basis for future structure-function studies of edible fungal polysaccharides in intestinal health. Download: Download high-res image (121KB) Download: Download full-size image
✓ 已验证
DOI
高影响因子
APPLIED BIOCHEMISTRY AND BIOTECHNOLOGY
·
2026
·
IF 3.3
Wang Zi-Xian,Huang Qiu-Ping,Wu Wei,Li Wan-Ying,Liu Jun-Yang,Wang Ke-Ying,Huang Chun-Xiang,Zhang Ming-Yu,Song Jia-Le
The aim of the present study was to investigate the effects of cyanidin-3,5-O-glucoside (C35G) on intestinal inflammation, mucosal barrier integrity, and fibrogenesis in a dextran sodium sulfate (DSS, 2.5%)-induced mouse model of ulcerative colitis (UC), as well as to elucidate the mechanisms underlying its effects. After a 28-day C35G intervention, UC mice showed significant improvements in clinical symptoms, including weight loss and an increased disease activity index (DAI). Additionally, there was an elevation in serum levels of inflammatory factors such as IL-1β, IL-6, IL-17 A, IL-18, and TNF-α. C35G increased the colonic mRNA levels of Zo1 , Claudin1 , and Occludin , and reduced intestinal epithelial permeability, ultimately promoting the restoration of mucosal barrier integrity in UC mice. In addition, C35G influenced the colonic Nrf2/Keap1 pathway by upregulating the mRNA levels of Cat , Sod1 , Sod2 , and Mgst1 . This modulation was accompanied by an increase in the serum levels of SOD and catalase, as well as a reduction in the levels of the oxidative stress marker MDA. The C35G-induced inhibition of NLRP3 inflammasome activation reduced the expression of intestinal fibrotic factors (α-SMA and Collagen I), ultimately attenuating intestinal fibrosis. Moreover, C35G stimulated autophagy in the intestinal epithelial tissues of UC mice by increasing the protein expression of LC3-II, Beclin 1, p-AMPK, and ULK1 while decreasing the levels of p62, p-Akt, and p-mTOR. These results suggested that C35G reduces oxidative stress and inflammation by acting as an antioxidant and modulating the Nrf2/Keap1 pathway. Additionally, C35G regulates autophagy through the AMPK/Akt/mTOR/ULK1 pathway, thereby improving intestinal inflammation, restoring the compromised intestinal barrier, and preventing intestinal fibrosis in mice with UC. Graphical
✓ 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）