CHEMICAL ENGINEERING JOURNAL
·
2025
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IF 13.2
Yifei Wang,Yaning Xia,Mengyang Zhou,Yong Zhang,Jingliang Cheng,Yupeng Shi
Oral drug delivery systems have great advantages in the treatment of enteritis. Compared to free drugs, the drug delivery system protects drugs from damage to the complex gastrointestinal environment and improves bioavailability. However, the limited accumulation of drugs in inflammatory bowel disease restricts the efficiency of oral drug delivery. Here, we propose an oral administration strategy to restore intestinal homeostasis by targeting the regulation of intestinal inflammation through biomimetic iron-tungsten nanomedicine guided by biological chemotaxis. The microcapsules introduce a lactic acid bacteria membrane giving the Fe/W-MOFs excellent resistance to the harsh gastrointestinal environment and improving their retention in the enteritis site. Furthermore, inspired by the hypoxic environment of the intestine and the symptoms of inflammatory bleeding, the microcapsules can be degraded in an anoxic response and release the corresponding iron, tungsten, and 5-ASA to achieve anemia treatment, intestinal flora regulation, and anti-inflammatory effects. It is worth noting that the effective release of iron ions can also be used as an MRI contrast agent for imaging and monitoring of enteritis treatment. Therefore, the biomimetic microcapsules can effectively and accurately reprogram the intestinal microbiome through a multi-pronged comprehensive treatment such as eliminating pathogenic bacteria, improving anemia, and anti-inflammation, bringing extraordinary advantages for diagnosing and treating DSS-induced colitis.
研究领域:
药学
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生物医学工程
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纳米医学
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胃肠病学
✓ 已验证
产品关联
DOI
高影响因子
Food & Function
·
2024
·
IF 5.1
Shumeng Hu,Runan Zhao,Tao Chen,Xuesong Chi,Yangjing Li,Di Wu,Bei-Wei Zhu,Jiangning Hu
The onset and progression of ulcerative colitis (UC) are intricately linked to the worsening of intestinal inflammation, an imbalance in oxidative stress, and impairment of the intestinal mucosal barrier. Although chlorogenic acid (CA) shows potential in effectively alleviating symptoms of UC, its clinical application is hindered by poor bioavailability, stability, rapid metabolism, and quick excretion. This study utilized a one-step enzyme-catalyzed polymerization technique to create chlorogenic acid nanoparticles (CA NPs), aiming to improve the bioavailability and stability of CA. The CA NPs exhibited an optimal nano size (106.65 ± 4.12 nm) and showed increased cellular uptake over time. Importantly, CA NPs significantly prolonged retention time in inflamed colonic tissues, enhancing accumulation and providing a targeted therapy for UC. Animal studies confirmed the substantial benefits of CA NPs, including reduced weight loss, lessened reduction in colon length, and a lowered disease activity index (DAI) score in DSS-induced UC mice. Moreover, CA NPs effectively reduced oxidative stress and levels of inflammatory factors in the colonic tissues of UC mice, thus mitigating tissue damage and restoring the integrity of the intestinal mucosal barrier. In conclusion, our research proposes a novel approach to increase the bioavailability and stability of CA, offering a promising avenue for its effective application in preventing UC.
研究领域:
药学
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纳米技术
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胃肠病学
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药理学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Frontiers in Nutrition
·
2024
·
IF 4
Shi Yuxuan,Guo Shasha,Zhou Jihong,Xu Ping,Wang Yuefei
Introduction: Black tea, a beverage consumed worldwide, possesses favorable effects on gastrointestinal tract, including nourishing stomach and promoting digestion. Nevertheless, its specific effects on intestinal homeostasis remains inconclusive.Methods: We applied black tea to mice prior to inducing colitis with DSS and then monitored their body weight and disease activity index (DAI) daily. When sacrificed, we measured intestinal permeability and conducted analyses of mucin and tight junction proteins. We detected inflammatory cytokines, immune cells, and related inflammatory signaling pathways. In addition, the gut microbiota was analyzed through 16S rRNA sequencing, and the concentrations of short-chain fatty acids (SCFAs) were also measured.Results: The results showed that black tea-treated group significantly rescued the DSS-disrupted intestinal structure. It reduced the relative abundance of the pathogenic bacterium Turicibacter, while increased the abundance of beneficial bacteria norank_f_Muribaculaceae and restored the contents of SCFAs such as acetate, propionate, and butyrate. It also protected the intestinal barrier by reducing the levels of immune response-related factors (e.g., TNF-α, IL-6, IL-1β) and increasing the expression of tight junction proteins (TJs) (e.g., ZO-1, occludin). Furthermore, black tea exhibited the capacity to suppress the expression of MMP-9 and ICAM-1, as well as to inhibit the activation of NF-κB signaling pathway.Discussion: Our findings provide a theoretical framework that elucidates the mechanisms by which black tea preserves intestinal homeostasis, highlighting its potential as a preventive strategy against intestinal disruptions. This study contributes to the understanding of the dietary effects of black tea on gastrointestinal health.
研究领域:
胃肠病学
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免疫学
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微生物学
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营养学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
·
2024
·
IF 5.7
Mengru Zhou,Xiaoyao Ma,Jiaqi Zhang,Xuan Lu
3,5-Dimethyl-8-methoxy-3,4-dihydro-1H-isochromen-6-ol (DMD) is a polyketide compound obtained from the endophytic fungus Penicillium sp. HJT-A-10 of Rhodiola tibetica. R. tibetica is a nourishing food and also used in traditional Chinese medicine and Xizang medicine. In dextran sulfate sodium (DSS)-induced ulcerative colitis (UC) mice, DMD significantly alleviated the pathological symptom of UC. Network pharmacology studies have shown that nucleotide-binding domain-like receptor family pyrin domain containing (NLRP) 3 is the primary target protein of DMD associated with anti-UC. In molecular biology studies, DMD suppressed the activation of NLRP3 and decreased the expression of downstream inflammatory proteins and pro-inflammatory cytokines in UC. The finding was further verified in knockout mice. DMD lost the effect of attenuating DSS-induced UC in NLRP3–/– mice. In conclusion, this study demonstrates that DMD reduces inflammatory response and balances the barrier integrity to attenuate UC via targeting NLRP3, and DMD is a potential natural agent or dietary supplement for attenuating UC.
研究领域:
药理学
·
免疫学
·
胃肠病学
·
分子生物学
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传统医学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
FOOD CHEMISTRY
·
2020
·
IF 6.306
Ruifeng Luo,Meisi Lin,Chen Zhang,Jinfeng Shi,Siyuan Zhang,Qiyan Chen,Yichen Hu,Minyue Zhang,Jinming Zhang,Fei Gao
Curcumin (CUR) is a promising edible phytochemical compound with ideal ulcerative colitis (UC) treatment activity; however, it is characteristically instable in the digestive tract and has a short retention time in colon. Therefore, we designed and fabricated an oral food-grade nanocarrier composed of tannic acid (TA)-coated, Genipin (Gnp)-crosslinked human serum albumin (HSA) to encapsulate CUR (TA/CUR-NPs). The resulting CUR nanoparticles (NPs) were about 220 nm and −28.8 mV. With the assistance of TA layer and Gnp-crosslinking, the entire nano-scaled system effectively delayed CUR release in simulated gastric fluid, prolonged its colon adhesion and increased its uptake in Caco-2 cells. As expected, TA/CUR-NPs oral administration significantly alleviated colitis symptoms in DSS-treated mice when compared with controls by inhibiting the TLR4-linked NF-κB signaling pathway. Collectively, this study indicates that we have developed a convenient, eco-friendly, nano-scaled vehicle for oral delivery of CUR with anti-UC benefit.
研究领域:
药学
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纳米技术
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药物递送系统
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胃肠病学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Journal of Advanced Research
·
2024
·
IF 11.4
Xue Bai,Zhiguang Duan,Jianjun Deng,Zhuo Zhang,Rongzhan Fu,Chenhui Zhu,Daidi Fan
Introduction Dysbiosis of the gut microbiota is emerging as a pivotal factor in the pathogenesis of colorectal cancer (CRC). Ginsenoside Rh4 (Rh4) is an active compound isolated from ginseng with beneficial effects in modulating intestinal inflammation and gut microbiota dysbiosis, but how Rh4 regulates the gut microbiota to alleviate CRC remains underexplored. Objectives We investigated the impact of Rh4 on CRC and the mechanism of its action in inhibiting CRC via modulation of gut microbiota. Methods We used the AOM/DSS model and employed transcriptomics, genomics and metabolomics techniques to explore the inhibitory impact of Rh4 on CRC. Furthermore, we employed experiments involving antibiotic treatment and fecal microbiota transplantation (FMT) to investigate the role of the gut microbiota. Finally, we elucidated the pivotal role of key functional bacteria and metabolites regulated by Rh4 in CRC. Results Our research findings indicated that Rh4 repaired intestinal barrier damage caused by CRC, alleviated intestinal inflammation, and inhibited the development of CRC. Additionally, Rh4 inhibited CRC in a gut microbiota-dependent manner. Rh4 increased the diversity of gut microbiota, enriched the probiotic Akkermansia muciniphila ( A. muciniphila ), and alleviated gut microbiota dysbiosis caused by CRC. Subsequently, Rh4 regulated A. muciniphila -mediated bile acid metabolism. A. muciniphila promoted the production of UDCA by enhancing the activity of 7α-hydroxysteroid dehydrogenase (7α-HSDH). UDCA further activated FXR, modulated the TLR4-NF-κB signaling pathway, thus inhibiting the development of CRC. Conclusion Our results confirm that Rh4 inhibits CRC in a gut microbiota-dependent manner by modulating gut microbiota-mediated bile acid metabolism and promoting the production of UDCA, which further activates the FXR receptor and regulates the TLR4-NF-κB signaling pathway. Our results confirm that Rh4 has the potential to be used as a modulator of gut microbiota for preventing and treatment of CRC.
研究领域:
癌症生物学
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微生物学
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药理学
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分子生物学
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胃肠病学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Journal of Functional Foods
·
2024
·
IF 3.8
Fang Shi,Yong-Sheng Gao,Shu-Mei Han,Huan Shi,Qing-Sheng Hou,Yang Gao,Xiao-Wen Wen,Zhen-Yu Zhu,Kai Liu,Wei-Peng Gong,Ben-Shi Wang,Xin Liu,Lei Zou
There is a growing amount of research that highlights the significant connection between the development of colitis and both metabolic imbalance and the inflammatory response. Tagatose, an inherent sweetening agent and alternative to sugar, plays a crucial role in the biosynthesis of several chemicals and metabolic pathways in living organisms. However, the specific biochemical mechanism via which tagatose hinders colitis is still not understood. According to recent study, tagatose plays a crucial role in safeguarding the integrity of tight junctions inside the intestinal mucosal barrier. Furthermore, it is crucial to acknowledge the presence of a correlation between the severity of inflammatory bowel disease (IBD) and the occurrence of colorectal cancer (CRC), chemically-induced colitis in rodents, and reduced blood levels of tagatose. The treatment of tagatose resulted in a decrease in intestinal mucosal injury in mice with colitis, regardless of whether it was caused by dextran sodium sulfate (DSS) or spontaneous colitis in IL-10 -/- mice and C3H/HeJBir mice. The introduction of tagatose in a colitis model triggers a cascade of events, wherein it hinders the expulsion of cathepsin B and enhances lysosomal cohesiveness. The aforementioned method successfully inhibits the activity of myosin light chain kinase (MLCK) in the context of intestinal epithelial damage, hence impeding the deterioration of tight junction integrity and the initiation of mitochondrial dysfunction. In summary, the outcomes of the study have provided empirical evidence that substantiates the beneficial effects of tagatose in mitigating the progression of colitis. The ability to prevent the disruption of the intestinal barrier is responsible for this achievement. Hence, tagatose has promise as a therapeutic adjunct for the management of colitis.
研究领域:
胃肠病学
·
药理学
·
免疫学
·
细胞生物学
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分子生物学
✓ 已验证
产品关联
DOI
高影响因子
Frontiers in Microbiology
·
2022
·
IF 6.064
Le Su,Feifan Ma,Zaiyong An,Xiuyu Ji,Ping Zhang,Qiulin Yue,Chen Zhao,Xin Sun,Kunlun Li,Baojun Li,Xinli Liu,Lin Zhao
Because of the increased incidence and prevalence, ulcerative colitis (UC) has become a global health issue in the world. Current therapies for UC are not totally effective which result in persistent and recurrent symptom of many patients. Lactobacillus with anti-inflammatory effects might be beneficial to the prevention or treatment for UC. Here, we examined the ameliorative effects of the metabolites of Lactobacillus fermentum F-B9-1 (MLF) in Caco-2 cells and dextran sodium sulfate (DSS)-induced UC model mice. MLF displayed intestinal barrier-protective activities in Caco-2 cells by increasing the expression of Occludin and ZO-1. They also showed anti-inflammatory potential in interleukin (IL)-1β and IL-6. In order to further examine the in vivo anti-inflammatory effect of MLF, the MLF was gavaged in the DSS-induced UC model mice. The intragastric administration of MLF effectively alleviated colitis symptoms of weight loss, diarrhea, colon shortening, and histopathological scores, protected intestinal barrier function by increasing Occludin and ZO-1, and attenuated colonic and systemic inflammation by suppressing production of IL-1β and IL-6. Finally, the use of MLF remodeled the diversity of the gut microbiota and increased the number of beneficial microorganisms. Overall, the results demonstrated that MLF relieved DSS-induced UC in mice. And MLF might be an effective therapy method to UC in the clinic in the future.
研究领域:
胃肠病学
·
微生物学
·
免疫学
·
药理学
✓ 已验证
DOI
PubMed
高影响因子
INTERNATIONAL IMMUNOPHARMACOLOGY
·
2023
·
IF 5.6
Minxuan Xu,Fang Shi,Yongshen Gao,Shumei Han,Chensuo Huang,Qinsheng Hou,Xiaoweng Wen,Bengshi Wang,Zhenyu Zhu,Lei Zou,Mingxin Xiong,Wei Dong,Jun Tan
There is a growing amount of research that highlights the significant involvement of metabolic imbalance and the inflammatory response in the advancement of colitis. Arabinose is a naturally occurring bioactive monosaccharide that plays a crucial role in the metabolic processes and synthesis of many compounds in living organisms. However, the more detailed molecular mechanism by which the administration of arabinose alleviates the progression of colitis and its associated carcinogenesis is still not fully understood. In the present study, arabinose is recognized as a significant and inherent protector of the intestinal mucosal barrier through its role in preserving the integrity of tight junctions within the intestines. Also, it is important to note that there is a positive correlation between the severity of inflammatory bowel disease (IBD) and colorectal cancer (CRC), as well as chemically-induced colitis in mice, and lower levels of arabinose in the bloodstream. In two mouse models of colitis, caused by dextran sodium sulfate (DSS) or by spontaneous colitis in IL-10 -/- mice, damage to the intestinal mucosa was reduced by giving the mice arabinose. When arabinose is administrated to model with colitis, it sets off a chain of events that help keep the lysosomes together and stop cathepsin B from being released. During the progression of intestinal epithelial injury, this process blocks myosin light chain kinase (MLCK) from damaging tight junctions and causing mitochondrial dysfunction. In summary, the results of the study have provided evidence supporting the beneficial effects of arabinose in mitigating the progression of colitis. This is achieved through its ability to avoid dysregulation of the intestinal barrier. Consequently, arabinose may hold promise as a therapeutic supplementation for the management of colitis.
研究领域:
胃肠病学
·
免疫学
·
分子生物学
✓ 已验证
DOI
PubMed
高影响因子
Journal of Advanced Research
·
2024
·
IF 11.4
Qin Yuan,Wen Liu,Wei Hao,Yi Chen,Yaqin Xiao,Hongyi Li,Mingju Shui,Ding-Tao Wu,Shengpeng Wang
Introduction Over decades, the source-function relationships of bioactive polysaccharides have been progressively investigated, however, it is still unclear how a defined structure may conduce to the bioactivities of polysaccharides. Objectives To explore the structure–function relationship of fungus polysaccharides, we employed a dextran sulfate sodium (DSS)‐induced colitis mouse model to compare the anti-inflammatory activity of two fungus polysaccharides from Dictyophora indusiata (DIP) and Tremella fuciformis (TFP), which exhibit distinct glycosidic linkages. Methods The structures of DIP and TFP were characterized through molecular weight detection, molecular morphology analysis, methylation analysis, and NMR analysis. Subsequently, we employed a DSS-induced colitis model to assess the anti-inflammatory efficacy of DIP and TFP. The colitis symptoms, histological morphology, intestinal inflammatory cytokines, and the composition and function of gut microbiota before and after polysaccharides treatment in colitis mice were also investigated. Results DIP, l,3-β-D-glucan with 1,4-β and 1,6-β-D-Glcp as branched chains, exhibited superior therapeutic effect than that of TFP consisted of a linear 1,3-α-D-mannose backbone with D-xylose and L-fucose in the side chains. Both DIP and TFP relieved DSS-induced colitis in a gut microbiota-dependent manner. Furthermore, metagenomics showed that DIP and TFP could partially reverse the bacterial function in colitis mice. Glycoside Hydrolase 1 (GH1) and GH3 were identified as being involved in hydrolyzing the glucose linkages in DIP, while GH92 and GH29 were predicted to be active in cleaving the α-1,3-linked mannose linkages and the glycosidic bonds of L-fucose residues in TFP. Conclusion Our findings highlight the pivotal role of glycosidic linkages in anti-inflammatory activities of fungus polysaccharides and would promote the design and discovery of polysaccharides with designated activity to be used as functional foods and/or therapeutics.
研究领域:
药理学
·
免疫学
·
微生物学
·
生物化学
·
分子生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
PHYTOMEDICINE
·
2024
·
IF 6.7
Ke Cai,Xin-Yue Cao,Fan Chen,Yue Zhu,Dong-Dong Sun,Hai-Bo Cheng,Jin-Ao Duan,Shu-Lan SU
ABSTRACT Background Xianlian Jiedu Decoction (XLJDD) has been used for the treatment of colorectal cancer (CRC) for several decades because of the prominent efficacy of the prescription. Despite the clear clinical efficacy of XLJDD, the anti-CRC mechanism of action is still unclear. Purpose The inhibitory effect and mechanism of XLJDD on CRC were investigated in the azoxymethane/dextran sulfate sodium (AOM/DSS)-induced mice. Methods The AOM/DSS-induced mice model was adopted to evaluate the efficacy after administering the different doses of XLJDD. The therapeutic effects of XLJDD in treating AOM/DSS-induced CRC were investigated through histopathology, immunofluorescence and ELISA analysis methods. In addition, metabolomics profile and 16S rRNA analysis were used to explore the effective mechanisms of XLJDD on CRC. Results The results stated that the XLJDD reduced the number of tumor growth on the inner wall of the colon and the colorectal weight/length ratio, and suppressed the disease activity index (DAI) score, meanwhile XLJDD also increased body weight, colorectal length, and overall survival rate. The treatment of XLJDD also exhibited the ability to lower the level of inflammatory cytokines in serum and reduce the expression levels of β -catenin, COX-2, and iNOS protein in colorectal tissue. The findings suggested that XLJDD has anti-inflammatory properties and may provide relief for those suffering from inflammation-related conditions. Mechanistically, XLJDD improved gut microbiota dysbiosis and associated metabolic levels of short chain fatty acids (SCFAs), sphingolipid, and glycerophospholipid. This was achieved by reducing the abundance of Turicibacter, Clostridium_sensu_stricto_1 , and the levels of sphinganine, LPCs, and PCs. Additionally, XLJDD increased the abundance of Enterorhabdus and Alistipes probiotics, as well as the content of butyric acid and isovaleric acid. Conclusion The data presented in this article demonstrated that XLJDD can effectively inhibit the occurrence of colon inner wall tumors by reducing the level of inflammation and alleviating intestinal microbial flora imbalance and metabolic disorders. It provides a scientific basis for clinical prevention and treatment of CRC.
研究领域:
肿瘤学
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药理学
·
微生物学
·
代谢组学
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免疫学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
CHEMICAL ENGINEERING JOURNAL
·
2025
·
IF 13.2
Mengyuan Qian,Min Ge,Shanshan Liu,Xin Wen,Ning Liu,Qianqian Wang,Jiaxu Cao,Xiuyan Jiang,Yan Zhang,Jun Yang,Lingyun Sun
Inflammatory bowel disease (IBD) is an incurable condition driven by chronic inflammatory dysregulation. Human mesenchymal stem cells (hMSCs) offer therapeutic promise, but limited persistence and functional heterogeneity constrain their clinical efficacy. Here, we present a bio-inspired priming platform built on poly(lactic- co -glycolic acid)/chitosan-heparin microparticles, engineered to display E/N-cadherin motifs and to enable controlled interleukin-1β release through PLGA biodegradation. These functionalized microparticles (hE/N-cad@P/C-h-IL-1β) assemble with hMSCs into hybrid aggregates that enhance cell survival under stress and improve adaptability to microenvironment cues. The priming process upregulates endogenous cadherin expression and modulates AKT/STAT signaling, conferring stimulus- and dose-responsive immune activity. In vitro , hybrid aggregates polarize macrophages toward an anti-inflammatory phenotype, expand regulatory T cells, and suppress pathogenic lymphocyte activation. In a dextran sulfate sodium (DSS) colitis model, intraperitoneal delivery of hybrid aggregates restores intestinal immune homeostasis, accelerates epithelial repair, and reduces disease severity to near baseline within fourteen days. By integrating cell-adhesive and cytokine signals within a modular platform, this strategy overcomes critical translational barriers in hMSC therapy and provides a blueprint for precisely targeted treatment of IBD and related inflammatory disorders.
研究领域:
再生医学
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免疫学
·
生物材料
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干细胞治疗
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炎症性疾病
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药物递送系统
✓ 已验证
产品关联
DOI
高影响因子
危险品化学品经营许可证（带存储）