Journal of Functional Foods
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2026
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IF 3.9
Zixuan Cui,Xiaojing Chen,Yufeng Wei,Danfei Huang,Chang Li
Jujube polysaccharides and nano‑selenium have gained attention for their bioactivity. This study used jujube polysaccharides to stabilize selenium nanoparticles (JP-SeNPs) via redox method. The optimized JP-SeNPs had an average size of 142.0 nm (PDI 0.1989), contained zero-valent selenium, showing no HepG2 toxicity at 5–40 μg/mL. In DSS-induced colitis mice, JP-SeNPs alleviated weight loss, disease activity, and colon shortening, reduced histopathological damage, restored goblet cells and tight junctions, and lowered colonic TNF-α, IL-1β, IFN-γ, and serum endotoxin. Cecal short-chain fatty acids (acetate, propionate, butyrate) rebounded. 16S rRNA sequencing revealed enhanced α-diversity, enrichment of butyrate-producers, and restored carbohydrate metabolism. JP-SeNPs ameliorate colitis via barrier repair, inflammation suppression, microbiota modulation, and SCFA promotion, supporting its development as a functional formulation.
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高影响因子
Foods
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2025
·Vol. 14
·期 18
·3279
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IF 5.1
Xiaoyan Feng,Hongbin Yuan,Tao You,Hengyi Xu
Secondary liver injury (SLI) is the most common complication in the development of inflammatory bowel disease (IBD), and it is susceptible to environmental factors, including diet patterns. As a food-brightening agent, titanium dioxide nanoparticles (TiO2NPs) are inevitably consumed by IBD patients. Currently, there are a few studies on TiO2NPs exposure to SLI in colitis mice. In this study, a SLI model was built using dextran sodium sulfate (DSS) free-drinking for 7 days after pre-exposure to TiO2NPs. The changes in the pathological results and liver function indicators suggested that high-dose TiO2NPs only exhibited a slight injury in the liver. With further analysis, we found that pre-exposure to high-dose TiO2NPs in mice with SLI led to an increase in intestinal permeability and hepatic LPS content, along with increased inflammatory cytokines and an anti-oxidative system imbalance. Subsequently, accumulated LPS and ROS overproduction activated the NOD-like receptor family pyrin-containing 3 (NLRP3) inflammasome, inducing hepatic cell pyroptosis. To provide compelling evidence, NLRP3 gene-deficient mice were used, and the results showed that the absence of NLRP3 improved liver function, alleviated hepatic inflammation, and reduced hepatic oxidative injury in SLI mice with TiO2NPs exposure. In summary, these results confirmed the critical role of the NLRP3 inflammasome in the TiO2NP-aggravated progression of SLI. Our study provided a comprehensive evaluation of foodborne nanoparticles on IBD complications, hoping that more studies can focus on IBD complications affected by environmental factors.
研究领域:
消化病学
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纳米毒理学
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免疫学
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分子生物学
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肝脏病学
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炎症性肠病
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环境与健康
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PubMed
高影响因子
Oxidative Medicine and Cellular Longevity
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2020
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IF 5.076
Bo Qian,Chengqiang Wang,Zhen Zeng,Yuan Ren,Dayu Li,Jia-Le Song
Ulcerative colitis is a chronic gastrointestinal disease characterized by intestinal inflammation and serious mucosal damage. As a naturally hydroxycinnamic acid, sinapic acid (SA) has antioxidant, anticancer, and neuroprotective activities. We investigated the anticolitic effect and potential mechanisms of SA in DSS-induced colitis in Kunming (KM) mice. SA treatment significantly reduced body weight loss, colon shortening, and intestinal wall thickening in colitis mice. SA treatment also significantly reduced the histological infiltration of inflammatory cells and decreased myeloperoxidase (MPO) activity in the colons of colitis mice. The administration of SA attenuated oxidative damage by enhancing the activity of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase and reduced the serum and colonic mRNA levels of proinflammatory cytokines in colitis mice. We used qRT-PCR and Western blotting assays and demonstrated that SA reduced the activation of the NLRP3 inflammasome and attenuated intestinal permeability by enhancing the expression of ZO-1, occludin, and claudin-1 in colitis mice. Here, we conclude that SA exhibits great anticolitic activity against DSS-induced colitis by enhancing the activity of antioxidant enzymes, reducing intestinal inflammation, and maintaining the intestinal barrier. Finally, we suggest that SA may be a safe adjuvant for the prevention of clinical colitis.
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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PubMed
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JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
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2023
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IF 6.1
Hai-Bo Huang,Wei Gong,Yi-Yang Hou,Wan-Ying He,Ran Wang,Xin-Chuang Wang,Jiang-Ning Hu
Mucoadhesive hydrogels with multifunctional properties such as gastric acid resistance and sustained drug release in the intestinal tract are highly desirable for the oral treatment of inflammatory bowel diseases (IBDs). Polyphenols are proven to have great efficacies compared with the first-line drugs for IBD treatments. We recently reported that gallic acid (GA) was capable of forming a hydrogel. However, this hydrogel is prone to easy degradation and poor adhesion in vivo. To tackle this problem, the current study introduced sodium alginate (SA) to form a gallic acid/sodium alginate hybrid hydrogel (GAS). As expected, the GAS hydrogel showed excellent antiacid, mucoadhesive, and sustained degradation properties in the intestinal tract. In vitro studies demonstrated that the GAS hydrogel significantly alleviated ulcerative colitis (UC) in mice. The colonic length of the GAS group (7.75 ± 0.38 cm) was significantly longer than that of the UC group (6.12 ± 0.25 cm). The disease activity index (DAI) value of the UC group was (5.5 ± 0.57), which was markedly higher than that of the GAS group (2.5 ± 0.65). The GAS hydrogel also could inhibit the expression of inflammatory cytokines, regulating macrophage polarization and improving the intestinal mucosal barrier functions. All these results indicated that the GAS hydrogel was an ideal candidate for oral treatment of UC.
研究领域:
药学
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生物医学工程
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胃肠病学
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PubMed
高影响因子
CHEMISTRY & BIODIVERSITY
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2025
·
IF 2.5
Qiaoying Song,xinyong You,xuexia Liu
The aim of this study was to comprehensively analyze the structural characteristics of Ziziphus jujuba dates polysaccharide (ZJP-I) and its potential activity against colitis in vivo. A series of advanced analytical techniques including ion exchange chromatography, gel column chromatography, infrared spectroscopy (IR), nuclear magnetic resonance (NMR) and scanning electron microscopy (SEM) were used to characterize the structure of ZJP-I. The results showed that the molecular weight of ZJP-I was 2.01×104 Da, and it was mainly composed of sugar residues T-D-Galp(1→, →4)-D-Glcp(1→, →3,6)-D-Glcp(1→ and →6)-D-Galp(1→ and →6)-D-Manp(1→. To appraise the potential efficacy of ZJP-I on colitis, in vivo experiments were executed by employing a murine colitis model elicited by DSS. The experimental results showed that ZJP-I could significantly improve the clinical symptoms of colitis mice, including weight loss and colon shortening. Further analysis showed that ZJP-I effectively inhibited intestinal inflammation and protected intestinal barrier function by regulating inflammatory cytokine homeostasis, alleviating oxidative stress and restoring secretion of short-chain fatty acids. These findings provided important theoretical basis and experimental support for the potential application of Ziziphus jujuba dates polysaccharides in functional food and medicine.
研究领域:
食品科学
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营养学
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药理学
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免疫学
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Journal of Translational Medicine
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2026
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IF 9.7
Fei Zou,Zengrong Wu,Su Wang,Mengmeng Xu,Pianpian Xia,Yaxian Hu,Tang Fang,Peijun Hu,Chongyang Huang,Feihong Deng
Background Intestinal barrier defects cause antigen translocation and immune dysregulation. The pyroptosis of colonic epithelial cells (CECs) disrupts the colonic barrier, and its inhibition might be a therapeutic approach for ulcerative colitis (UC), but the mechanisms are not fully understood. Methods A DSS-induced UC model was established to assess the level of colonic epithelial cell pyroptosis. 16S rDNA sequencing and LC‒MS/MS were applied to screen potential candidate bacterial species and metabolites. The roles of target metabolites were evaluated in vivo using GSDMD-knockout mice. FHC cells treated with LPS + ATP were used as a cellular model of pyroptosis, and the underlying molecular mechanism was explored mainly by siRNA transfection and lentivirus infection. Results We found that DSS-treated mice exhibited increased levels of pyroptosis in the colon. Fecal microbiota transplantation (FMT) significantly suppressed mucosal inflammation and CEC pyroptosis, accompanied by increased levels of butyrate-producing bacteria and butyrate in feces. Butyrate treatment alleviated DSS-induced colitis in mice. Moreover, GSDMD knockout mitigated DSS-induced colitis in mice, whereas a butyrate intervention failed to further ameliorate colitis in GSDMD-knockout mice. Mechanistically, we found that butyrate significantly inhibited LPS + ATP-induced pyroptosis by activating its receptor, aryl hydrocarbon receptor (AhR), in FHC cells, while silencing AhR suppressed this effect. The overexpression of cGAS in FHC increased the level of pyroptosis, whereas the administration of butyrate inhibited the activation of the cGAS–STING pathway. Treatment with a cGAS inhibitor significantly reversed the increase in pyroptosis caused by AhR knockdown in pyroptotic FHC cells. Conclusions Gut microbiota-derived butyrate levels were increased after FMT. Butyrate suppressed the proinflammatory cGAS–STING–NF-κB signaling axis via AhR to inhibit CEC pyroptosis and thereby alleviate UC. Supplementary Information The online version contains supplementary material available at 10.1186/s12967-026-08264-1.
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COLLOIDS AND SURFACES B-BIOINTERFACES
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2026
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IF 5.6
Jianye Li,Ruigang Zhou,Jiali Huang,Jing Cheng,Haibo Liu,Fanghong Chen,Jianxin Ma,Junjie Huang
Gallic acid (GA), recognized for its antioxidant and anti-inflammatory bioactivities, has demonstrated efficacy in ameliorating experimental colitis. However, its clinical translation is impeded by poor water solubility. Deep eutectic solvents (DESs), as environmentally friendly green solvent systems, have emerged as promising candidates to address this limitation. Hydrogels are considered a viable strategy to enhance the anti-colitis efficacy of GA. The hydrogel (PC-CuGA) was fabricated using a one-step mixing method and cross-linked through non-covalent interactions by DES, polyvinyl alcohol (PVA), chitosan (CS), GA, and Cu 2 + . Additionally, DSS-evoked colitis was established and applied to clarify the regulatory efficacy of PC-CuGA on intestinal barrier impairment, inflammatory response, and redox imbalance. Results revealed that PC-CuGA exhibited a robust gel state with excellent temporal stability, superior storage modulus, enhanced structural integrity, and favorable biosafety. In the colitis model, PC-CuGA intervention effectively mitigated DSS-induced pathology, as evidenced by reduced weight loss, attenuated colon shortening, and lowered disease activity index (DAI) scores. Histopathological analysis further demonstrated that PC-CuGA preserved intestinal barrier integrity and protected tight junction proteins. Mechanistically, PC-CuGA significantly dampened the activation of the TLR4/MyD88/NF-κB axis and downregulated the expression of pro-inflammatory cytokine genes, while upregulating the expression of anti-inflammatory cytokines. Collectively, these findings elucidate that the protective effects of PC-CuGA against experimental colitis associated with reinforcing intestinal barriers, suppressing oxidative stress, and excessive inflammation. This work provides a novel therapeutic strategy for the prevention and management of colitis, highlighting the potential of DES-based hydrogels in enhancing the bioavailability and efficacy of bioactive compounds.
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BIOORGANIC CHEMISTRY
·
2026
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IF 5.1
Yinyue Wang,Ruyi Zhang,Yangjiao Xu,Hongtao Shi,Xueyao Hu,Nairong Yu,Yu-Qiang Zhao,Baomin Fan,Guangzhi Zeng
NCTD-01 shows anti-inflammatory and cytotoxic effects in vitro and in vivo. • NCTD-01 exhibits low in vivo toxicity and a high oral MTD. • NCTD-01 suppresses AOM/DSS-induced colorectal cancer safely in mice. • NCTD-01 limits inflammation-to-cancer transition via NF-κB and Treg regulation. Although cantharidin (CTD) exhibits significant clinical efficacy against various cancers, its clinical utility is severely hampered by profound systemic toxicity. Thus, structural modification of CTD to obtain analogues with potent anticancer activity and lower toxicity is essential for advancing CTD-based therapeutics. Building on our previous synthesis of a series of C-5 alkynyl-substituted CTD analogues with potent anti-inflammatory properties, this study investigates the anticancer potential of a new analogue NCTD-01 demonstrated a favorable safety profile in mice, with the maximum tolerated dose (MTD) for oral administration exceeding 1852 mg/kg. In addition to exhibiting potent in vitro and in vivo anti-inflammatory activities comparable to its analogues, NCTD-01 displayed cytotoxicity against colon cancer cell lines and exhibited therapeutic efficacy in an azoxymethane/dextran sulfate sodium-induced orthotopic mouse model of colorectal cancer. Molecular analyses revealed that NCTD-01 reduced Ki-67 expression, suppressed the mRNA levels of pro-inflammatory and immunosuppressive mediators ( IL-1β , COX-2 , IL-6 , IL-10 , and TGF-β ) in colonic tumor tissues, and decreased serum levels of TNF-α and IL-1β. Furthermore, NCTD-01 treatment led to reduced expression of Foxp3, CD25, PD-1, and PD-L1, alongside enhanced CD8 and GITR expression in colorectal tissues, suggesting an effective modulation of tumor-associated immune responses. This study suggests that NCTD-01, a new C-5 alkynyl-substituted CTD analogue, may help alleviate the inflammation-to-cancer transition through tumor-associated immune modulation while maintaining a favorable safety profile, pointing to its potential as a candidate for anticancer drug discovery. Download: Download high-res image (99KB) Download: Download full-size image
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IMMUNOBIOLOGY
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2024
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IF 2.5
Dan Gu,Ting Cao,Shijie Yi,Xiaoqian Li,Ya Liu
Background We have previously found that enhancer of zeste homolog 2 (EZH2) is correlated with inflammatory infiltration and mucosal cell injury in ulcerative colitis (UC). This study aims to analyze the role of X-inactive specific transcript (XIST), a possible interactive long non-coding RNA of EZH2, in UC and to explore the mechanisms. Methods C57BL/6N mice were treated with dextran sulfate sodium (DSS), and mouse colonic mucosal epithelial cells were treated with DSS and lipopolysaccharide (LPS) for UC modeling. The UC-related symptoms in mice, and the viability and apoptosis of mucosal epithelial cells were determined. Inflammatory injury in animal and cellular models were assessed through the levels of ACS, occludin, IL-1β, IL-18, TNF-α, caspase-1, and caspase-11. Molecular interactions between XIST, EZH2, and GABA type A receptor-associated protein (GABARAP) were verified by immunoprecipitation assays, and their functions in inflammatory injury were determined by gain- or loss-of-function assays. Results XIST was highly expressed in DSS-treated mice and in DSS + LPS-treated mucosal epithelial cells. It recruited EZH2, which mediated gene silencing of GABARAP through H3K27me3 modification. Silencing of XIST alleviated body weight loss, colon shortening, and disease active index of mice and reduced inflammatory injuries in their colon tissues. Meanwhile, it reduced apoptosis and inflammation in mucosal epithelial cells. However, these alleviating effects were blocked by either EZH2 overexpression or GABARAP knockdown. Rescue experiments identified caspase-11 as a key effector mediating the inflammatory injury following GABARAP loss. Conclusion This study suggests that the XIST-EZH2 interaction-mediated GABARAP inhibition activates caspase-11-dependent inflammatory injury in UC.
研究领域:
分子生物学
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免疫学
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胃肠病学
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PubMed
高影响因子
BIOCHEMICAL PHARMACOLOGY
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2023
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IF 5.8
Zhen Qiao,Min Liao,Mingyue Xiao,Saiyan Luo,Kexin Wang,Mengxin Niu,Honglv Jiang,Suya Sun,Guoqiang Xu,NanJie Xu,Qiongming Xu,Yanli Liu
Ephrin B3 , a member of Eph/ephrin family, contributes to embryogenesis and carcinogenesis, but few studies have suggested whether this ligand has regulatory effect on colitis . This study was to determine whether ephrin B3 played a role in colitis and colonic carcinogenesis. Dextran sodium sulfate (DSS)-induced colitis and azoxymethane (AOM)/DSS-induced colitis-associated carcinogenesis model was established in Efnb3 -deficient ( Efnb3 −/− ) mice. Label-free quantitative proteomics were performed to identify the Efnb3- regulated proteins. Our results showed that Efnb3 knock out reduced the symptoms of DSS-induced colitis, such as disease activity index (DAI), inflammatory factors release, and dysfunction of the intestinal barrier. Quantitative proteomics revealed that Efnb3 regulated 95 proteins which clustered in the platelet degranulation, response to elevated platelet cytosolic Ca 2+ , MAPK signaling for integrins such as ITGB4. Furthermore, ephrin B3 inactived ITGB4/AKT signal pathway and then promoted epithelial barrier dysfunction. Simultaneously, ephrin B3 promoted Gremlin-1/NF-κB signal pathway and thereby increased inflammatory factors release. In addition, the higher level of Efnb3 in colon cancer patients is correlated with worse survival. Efnb3 −/− mice exhibited susceptibility to AOM/DSS-induced colorectal cancer . Our finding discovered that Efnb3 played an important role in the development of colitis and colitis-associated colorectal cancer. Efnb3 deficiency improved the intestinal barrier by ITGB4 and suppressed inflammation via Gremlin-1/NF-κB signal pathway, which may provide a novel therapeutic strategy for the treatment of colitis and colitis-associated colorectal cancer.
研究领域:
免疫学
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肿瘤学
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分子生物学
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胃肠病学
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PubMed
高影响因子
Food Quality and Safety
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2025
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IF 4.4
Ye Hongling,He Yaling,Jin Mingzhi,Ye Ziyang,Huang Qianli,Chen Hui,Ye Ming
Ulcerative colitis is a common inflammatory bowel disease. This study evaluated the protective effect and potential mechanism of Stropharia rugosoannulata polysaccharide (SP-1a) and its carboxymethylated and phosphorylated derivatives (CSP-1a and PSP-1a) against dextran sulfate sodium (DSS)-induced ulcerative colitis. The results showed that treatment with SP-1a and its derivatives alleviated the symptoms of weight loss, colon shortening, and blood in the stool induced by . SP-1a and its derivatives restore the integrity of the intestinal barrier by controlling the expression of tight junction proteins. Furthermore, they play an anti-inflammatory role by reducing oxidative stress and inhibiting the expression of pro-inflammatory factors, pro-inflammatory proteins, and nuclear factor kappa-B (NF-κB) signaling pathways. The anti-inflammatory effects of CSP-1a and PSP-1a were greater than those of SP-1a. These results indicate that SP-1a could be a potential natural medicine to protect against DSS-induced colitis.
研究领域:
医学
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免疫学
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分子生物学
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高影响因子
Chinese Herbal Medicines
·
2025
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IF 8.9
Wen Liu,Biqiong Zhang,Zhengxi Hu,Si Yao,Yunpeng Zhao,Fengqing Wang,Yuanyuan Wang,Xinxin Yang,Jie Yin,Weiguang Sun,Qingyi Tong,Lianghu Gu,Yonghui Zhang
Objective To design and synthesize an amount of butyrolactone V derivatives, evaluate the anti-inflammatory effects of all the derivatives, look for potential drugs that inhibit inflammatory bowel disease (IBD), and determine the structure–activity relationship (SAR). Methods The butyrolactone V derivatives were synthesized with high yield by oxidation reaction, substitution reaction, and esterification reaction in sequence, and the production of nitric oxide was assessed in RAW264.7 cells treated with the lipopolysaccharide and the compounds. Then, the target compounds were studied for their activity in dextran sodium sulfate (DSS)-induced ulcerative colitis. Results A total of three series of compounds encompassing 60 derivatives of the natural product butyrolactone V were designed and synthesized. The results showed that compounds 5p and 7e could alleviate the symptoms of DSS-induced colitis in mice, including alleviating diarrhea, inhibiting the reduction of colon length, and reducing tissue damage. The preliminary mechanism exploration indicated that compounds 5p and 7e could improve the symptoms of IBD in mice mainly by reducing the expression of chemokines and exerting anti-inflammatory effects. Conclusion This study reports the synthesis and the derivatization of butyrolactone V and analysis on anti-inflammatory activity. The most effective compounds 5p and 7e have the potential to be further developed as drugs to treat IBD.
研究领域:
药理学
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有机合成化学
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炎症研究
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PubMed
高影响因子
危险品化学品经营许可证（带存储）