JOURNAL OF ETHNOPHARMACOLOGY
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2024
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IF 4.8
Li-Ying Han,Hao Yu,Shuai Wang,Yong-Rui Bao,Tian-Jiao Li,Ying Zheng,Xi Luo,Meng-Nan Jia,Qiang Zhang,Xian-Sheng Meng
Ethnopharmacological relevance Colorectal cancer (CRC) belongs to the category of intestinal wind, anal ulcer, abdominal mass and other diseases in traditional Chinese medicine (TCM). Floris Sophorae Powder (F.S), is a classical prescription is recorded in Puji Benshi Fang for the treatment of intestinal carbuncle. It has been incorporated into the prescriptions for the treatment of intestinal diseases and achieved remarkable results in modern medicine. However, the mechanism of F.S in the treatment of colorectal cancer remains unclear and requires further study. Aim of the study To investigate F.S in treating CRC and clarify the underlying mechanism. Materials and methods This study was based on Dextran Sulfate Sodium Salt (DSS) combined with Azoxymethane (AOM) induced CRC mouse model to clarify the pharmacological effects of F.S. The serum metabolomics was used to study the mechanism of action, and the chemical composition of F.S was found by UPLC-Q-TOF-MS. The rationality of serm metabolomics results was verified through the clinical target database of network pharmacology, and the upstream and downstream targets of related pathways were found. The mechanism pathway was verified by Western blot to clarify its mechanism of action. Results In vivo pharmacological experiments showed that F.S inhibited tumor growth and improved hematochezia. The vital signs of mice in the high-dose F.S group approached to those in the control group. A total of 43 differential metabolites were found to be significantly changed by serum metabolomics. F.S could modulate and recover most of the differential metabolites, which proved to be closely related to the KRAS/MEK-ERK signaling pathway. A total of 46 compounds in F.S were identified, and the rationality of serm metabolic pathway was verified by network pharmacology. Western blot results also verified that the expression of KRAS, E2F1, p-MEK and p-ERK were significantly decreased after F.S treatment. Conclusion Classical prescription Floris Sophorae Powder treat colorectal cancer by regulating KRAS/MEK-ERK signaling pathway.
研究领域:
药理学
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肿瘤学
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中医
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代谢组学
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信号转导
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PubMed
高影响因子
Journal of Inflammation Research
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2025
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IF 4.1
Yinyin Zhao,Binyuan Jiang,Shengnan Zuo
Purpose Cucurbitacins have demonstrated anti-inflammatory effects and show promise for inflammatory bowel diseases. However, the underlying mechanisms by which cucurbitacins affect colitis remain largely unknown.Methods In this study, we investigated the impact of cucurbitacin IIa on dextran sulfate sodium (DSS)-induced colitis in rats and the alterations in intestinal extracellular vesicles (EVs). EVs were isolated and characterized, followed by analysis of the small RNAs and proteins encapsulated within them using small RNA sequencing and proteomics, respectively.Results Our results revealed that cucurbitacin IIa alleviated colitis symptoms in DSS-treated rats, along with changes in the morphology and composition of intestinal EVs. Notably, EVs from cucurbitacin IIa-treated rats also mitigated colitis symptoms in DSS-treated rats. Further analysis showed that cucurbitacin IIa modified the protein profiles and microRNA composition of EVs extracted from the feces of colitis rats. Specifically, microRNA-30b-5p, significantly increased by cucurbitacin IIa, was found to alleviate colitis symptoms in DSS-treated rats. In conclusion, cucurbitacin IIa appears to alleviate colitis by promoting the release of microRNA-30b-5p from host-derived extracellular vesicles.Conclusion These findings enhance our understanding of cucurbitacin IIa’s effects on intestinal health and offer potential new therapeutic targets for inflammatory bowel disease treatment.
研究领域:
药理学
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胃肠病学
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分子生物学
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DOI
PubMed
高影响因子
Food & Function
·
2021
·Vol. 12
·期 11
·5171-5186
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IF 5.396
Bing Pang,Han Jin,Ning Liao,Junjun Li,Chunmei Jiang,Dongyan Shao,Junling Shi
Gut microbiota imbalance is one of the major causes of ulcerative colitis (UC). L. rhamnosus SHA113 (LRS), a strain isolated from healthy human milk, influences the regulation of gut flora. This study aims to determine whether this strain can ameliorate UC by modulating gut microbiota. Mouse models of UC were established using C57BL/6Cnc mice with intragastric administration of 3.0% (w/v) dextran sodium sulfate (DSS). LRS was used to treat the mouse models of UC with 109 cfu mL−1 cell suspension via intragastric administration. To verify the effect of gut microbiota on UC, fecal microbiota collected from the mice after the treatment with LRS were also used to treat the UC mouse models (FMT). The severity of UC was evaluated based on body weight, colon length, disease activity index (DAI), and hematoxylin–eosin staining. The microbial composition was analyzed by 16S rRNA sequencing. The mRNA expression levels of cytokines, mucins, tight junction proteins, and antimicrobial peptides in the gastrointestinal tract were detected by quantitative real-time polymerase chain reaction. The short-chain fatty acid (SCFAs) in the cecal contents of all mice were quantitatively detected by gas chromatography and mass spectrometry. Both LRS and FMT exerted excellent therapeutic effects on UC, as evidenced by the reduction in body weight loss, colon length, and colon structural integrity, as well as the increase in the DAI (disease activity index). LRS and FMT treatments showed similar effects: (1) an increase of total SCFA production in the cecal contents and the abundance of gut microbial diversity and flora composition; (2) decreases in two genera (Parabacteroides and Escherichia/Shigella) related to the DAI and the enhancement of SCFAs and IL-10 positively related genera in the gut microbiota (Bilophila, Roseburia, Akkermansia, and Bifidobacterium); (3) downregulation of the expression of tumor necrosis factor-α, interleukin IL-6, and IL-1β, and upregulation of the expression of the anti-inflammatory cytokine IL-10; and (4) upregulation of the expression of mucins (Muc1–4) and tight junction protein ZO-1. Overall, L. rhamnosus SHA113 relieves UC via the regulation of gut microbiota: increases in SCFA-producing genera and decreases in UC-related genera. In addition, a single strain is sufficient to induce a significant change in the gut microbiota and exert therapeutic effects on UC.
研究领域:
微生物学
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免疫学
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胃肠病学
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DOI
PubMed
高影响因子
AMERICAN JOURNAL OF CHINESE MEDICINE
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2022
·Vol. 51
·期 01
·107-127
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IF 6.005
Li Wang,Li Shao,Man-Yun Chen,Lin Wang,Pu Yang,Feng-Bo Tan,Wei Zhang,Wei-Hua Huang
Gut microbiota are significantly associated with the occurrence and development of inflammatory bowel disease (IBD). Panax notoginseng saponins (PNS) could be used for colitis and to modulate gut microbiota. However, the mechanism behind the effects of PNS on anti-colitis that are pertinent to gut microbiota is largely unknown. This study aimed to evaluate the anti-colitis effects of PNS and explore the involved mechanism as it is related to gut microbiota. Results showed that PNS significantly alleviated dextran sulfate sodium (DSS)-induced colitis. Meanwhile, after PNS treatment, the tight junction proteins were enhanced and proinflammatory cytokines, such as TNF- α , IL-6, IL-1 β , and IL-17, were decreased. Furthermore, Bacteroides spp. were significantly increased after modeling, while PNS reduced their abundance and significantly increased the amount of Akkermansia spp. in vivo . Importantly, Akkermansia spp. and Bacteroides spp. were correlated with the IBD disease indicators. Moreover, fecal microbiota transplantation (FMT) experiments confirmed that PNS-reshaped gut microbiota significantly alleviated DSS-induced colitis, while A. muciniphila significantly reduced the levels of the LPS-induced cellular inflammatory factors IL-1 β and TNF- α . In conclusion, PNS alleviated colitis pertinent to the upregulation of Akkermania spp. and downregulation of Bacteroides spp . in the gut.
研究领域:
药理学
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微生物学
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胃肠病学
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PubMed
高影响因子
JOURNAL OF BIOMOLECULAR STRUCTURE & DYNAMICS
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2023
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IF 4.4
Weiqin Wang,Xuefeng Li,Hangyi Wu,Fanli Shi,Zhenhai Zhang,Huixia Lv
The incidence of ulcerative colitis (UC) is rising worldwide. As a refractory and recurrent disease, UC could seriously affect the patients’ quality of life. However, current clinical medical treatments for UC are accompanied by various side effects, especially for long-term applications. Here, the underlying efficacy of cyclodextrins (CDs) was studied. As common excipients, CDs endow proven safety for long-term applications. Results of predictive methods derived from network pharmacology prompted the potential anti-inflammatory effects of CDs by oral administration. RAW264.7 cell experiments verified that CDs could inhibit the excessive secretion of TNF-α (β-CD > α-CD ≈ γ-CD), IL-6, and NO (α-CD > β-CD ≈ γ-CD) as predicted. In mice with DSS-induced acute UC, oral administration of CDs could effectively mitigate the pathological damage of colon tissue and reduce the level of inflammatory mediators. Moreover, 16S rRNA sequencing displayed that gut microbes disturbed by DSS were significantly regulated by CDs. Conclusively, the study showed the therapeutic application prospects of CDs in UC treatment and indicated the feasibility and advantages of developing ‘new’ therapeutic activities of ‘old’ ingredients.Communicated by Ramaswamy H. Sarma
研究领域:
药理学
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炎症
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胃肠病学
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微生物学
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DOI
PubMed
高影响因子
JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
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2023
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IF 6.1
Nan Li,Ruiyan Wang,Wenwen Li,Qian Du,Zeyuan deng,Yawei Fan,Liufeng Zheng
Vitexin, which exists in various medicinal plants and food sources, has recently received increasing attention because of its anti-inflammatory properties. This study aims to identify the protein target of vitexin that ameliorates dextran sulfate sodium (DSS)-induced colitis. The results showed that vitexin not only alleviated the clinical symptoms and colonic damage in mice with DSS-induced colitis but also suppressed the colonic production of inflammatory cytokines (IL-1β, IL-6, ICAM, and VCAM) and enhanced the expression of barrier-associated proteins (ZO-1, Occludin, and E-cadherin). Based on tissue thermal proteome profiling (Tissue-TPP) and molecular docking, OLA1 was creatively identified as a potential protein target for vitexin. Further siRNA-mediated knockdown of the OLA1 gene in Caco-2 cells demonstrated the ability of OLA1 to increase Nrf2 protein expression and, thus, mediated the anti-inflammatory effects of vitexin. Interaction of the OLA1–vitexin complex with Keap1 protein to disrupt the Keap1-Nrf2 interaction may be required for activating Nrf2. Our findings revealed a novel role for OLA1 as a protein target of vitexin that contributes to its anti-inflammatory action by activating Nrf2, which may provide a promising molecular mechanism for novel therapeutic strategies to treat colitis and the associated systemic inflammation.
研究领域:
药理学
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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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产品关联
DOI
PubMed
高影响因子
Journal of Pharmaceutical Analysis
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2026
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IF 11.2
Luyun Yang,Yingchao Li,Chunyan Yin,Litao Wu,Kexin Cheng,Jiafu Liang,Xiaona Cheng,Quan Zhang,Yakun Huang,Haoyun Bai,Wenlong Wang,Kaikai Lu,Rong Zhao,Zizhen Guo,Mingzhen Zhang,Shengli Han,Dongmin Li
Inflammatory bowel disease (IBD) is a chronic intestinal inflammatory condition resulting from complex interactions. With current clinical treatments showing limited efficacy, IBD poses an increasing global health challenge. Analysis of the GEO database, clinical samples from IBD patients, and a dextran sulfate sodium (DSS)-induced murine colitis model consistently reveal elevated Toll-like receptor 2 (TLR2) expression at both transcriptional and protein levels, implicating it in IBD pathogenesis and highlighting its potential as a therapeutic target. Previous studies have shown that Schisandrin B (SchB) protects DSS-induced colitis, but whether it directly targets an upstream immune receptor such as TLR2, and what additional mechanisms beyond its known anti-inflammatory actions exist, remain to be explored. In this study, SchB is identified as a moderate TLR2 ligand using cell membrane chromatography (CMC). By directly binding to TLR2 and inhibiting its heterodimerization with Toll-like receptor 1 (TLR1) or Toll-like receptor 6 (TLR6), SchB exerts significant anti-inflammatory and therapeutic effects in inflammatory cell models and ameliorates both DSS-induced ulcerative colitis and peptidoglycan (PGN)-induced immune colitis in mice. SchB inhibits TLR2 signaling and activates the sequestosome 1 (p62/SQSTM1)/Kelch-like ECH-associated protein 1 (Keap1)/nuclear factor erythroid 2-related factor 2 (Nrf2) axis, concurrently exerting anti-inflammatory, antioxidant, and anti-apoptotic effects and reinforcing intestinal barrier integrity. These findings provide new evidence of molecular mechanisms supporting SchB as a promising therapeutic candidate for IBD.
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DOI
高影响因子
BMC MICROBIOLOGY
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2025
·Vol. 25
·期 1
·1-19
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IF 4.2
Xu Zeyan,Zhao Lijiang,Wu Mengting,Cui Anqi,Chen Wei,Zheng Guohao,Zhou Jingyi,Gao Daqing,Shi Ruihua
Background Inflammatory bowel disease (IBD) involves the complex interplay among the mucosal barrier, microbiota, immunity and genetic factors. There are currently no satisfactory treatments for IBD. Administration of the probiotic Bacillus licheniformis (Bl) can improves colitis by regulating the gut microbiota. The phytohormone abscisic acid (ABA) treatment has favorable effects on immunity, as well as on inflammatory diseases like colitis. We hypothesized that the expression of an additional cyp gene by the Bl to increase its ABA production would enhance its effects. Results In this study, we found that a Bl-cyp strain overexpressing the cyp gene secreted more ABA into its supernatant than either the parental Bl stain or a Bl-pET82a strain expressing only a vector pET82a when these bacteria were grown in Nfb medium for 48 h. The prophylactic administration of the Bl-cyp strain culture more effectively attenuated dextran sodium sulfate (DSS)-induced colitis in mice compared to the Bl and Bl-pET28a strains. These findings were associated with significantly reduced epithelial barrier damage, as well as increased number of goblet cells and expression levels of occludin gene in the colonic epithelial layer, and decreased serum LPS levels in the Bl-cyp group. In addition, the administration of Bl-cyp strain effectively regulated the disordered gut microbiota by improving their diversity, richness and compositions more than the Bl or Bl-pET82a strain, including the ratio of Bacteroidota : Bacillota . It also inhibited the excessive growth of opportunistic pathogen Escherichia just like the Bl or Bl-pET82a strain. Moreover, the preventive administration of the Bl-cyp strain to mice following DSS-induced colitis enhanced the proportion of Treg cells and suppressed the proportion of Th17 cells in mesenteric lymph nodes (MLNs), decreased the levels of pro-inflammatory cytokines TNF-α, IL-6, and IL-22, and increased the level of anti-inflammatory IL-10 in colon tissues, similar to treatment with a high concentration of the ABA standard (ABA-H). Notably, the treatment with the Bl-cyp strain more effectively regulated the disordered microbiota than the ABA-H. Conclusions The administration of the Bl-cyp strain may provide a novel preventive approach for IBD, and may exert its effects by modulating the gut microbiota and host’s immune status.
研究领域:
微生物学
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免疫学
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消化系统疾病
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DOI
PubMed
高影响因子
Food Science and Human Wellness
·
2024
·
IF 5.6
Yu Peng,Xiaoao Xiao,Tingting Ji,Xinyuan Wang,Yixuan Xu,Jianbo Xiao,Hui Cao,Zhiyong Chen,Huifan Liu,Yuanqing Gao,Hongxun Tao
Rhodiola crenulate is the edible medicinal herbal medicine widely used for altitude sickness in China. Interestingly, our previous work has found that R. crenulate extract (RCE) could significantly improve the pathology associated with dextran sulfate sodium-induced colitis. Thus, the current research aims to reveal the pharmacodynamic material basis of RCE, as well as its mechanism against colitis. The chemical characterization of RCE was performed by UHPLC-HR-MS, through which a total of 88 constituents were identified. Meanwhile, our results also found 29 constituents absorbed into blood and 8 metabolized absorbable compounds. The decreased flavonoids prototype and the elevated sulfated products of phenols were observed under pathophysiological conditions of colitis. The metabolomics study revealed that colitis caused the alternation of fatty acid metabolism, steroid hormone biosynthesis and bile acid metabolism. Correspondingly, RCE could prevent colitis by improving fatty acid metabolism and secondary bile acid metabolism.
研究领域:
药理学
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植物化学
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代谢组学
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DOI
高影响因子
JOURNAL OF ETHNOPHARMACOLOGY
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2022
·
IF 5.195
Zhenhua Bian,Yuwen Qin,Lin Li,Lianlin Su,Chenghao Fei,Yu Li,Minmin Hu,Xiaowei Chen,Wei Zhang,Chunqin Mao,Xiaohang Yuan,Tulin Lu,De Ji
Ethnopharmacological relevance the fruit of Schisandra chinensis (Turcz.) Baill. (SC) is an important traditional Chinese herbal medicine, which has been widely used in traditional Chinese medicine (TCM) for treating intestinal diseases . It is also traditionally used as health product and medicine in Russia and other countries. However, the effect of SC ethanol extract on anti-ulcerative colitis (UC) has not been systematically studied yet. Aim of the study We investigated the protective effects and underlying action mechanisms of SC extract (SCE) for UC treatment. Materials and methods An animal model of UC induced by dextran sulfate sodium (DSS) was established. After oral administration of SCE, the Disease Activity Index (DAI) was calculated, the length of colon measured, levels of proinflammatory factors determined, and histopathology carried out to assess the therapeutic efficacy of SCE on UC. The effects of SCE on the toll-like receptor 4/nuclear factor-kappa B/nucleotide-binding and oligomerization domain-like receptor family pyrin domain containing 3 inflammasome (TLR4/NF-κB/NLRP3 inflammasome) signaling pathway were evaluated by western blotting . High-throughput sequencing was done to reveal the effect of SCE on the change of the gut microbiota (GM) in mice with DSS-induced colitis. Results SCE significantly reduced the DAI score, restored colon-length shortening, and ameliorated colonic histopathologic injury in mice with DSS-induced colitis. SCE inhibited the inflammatory response by regulating the TLR4/NF-κB/NLRP3 inflammasome pathway in mice with UC. SCE also maintained gut barrier function by increasing the levels of zonula occludens (ZO)-1 and occludin . 16S rRNA sequencing showed that SCE could reverse the GM imbalance caused by UC. Conclusions SCE can ameliorate DSS-induced colitis, and that its effects might be associated with suppression of the TLR4/NF-κB/NLRP3 inflammasome pathway and GM regulation, which may provide significant supports for the development of potential candidates for UC treatment.
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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传统中医
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DOI
PubMed
高影响因子
FOOD CHEMISTRY
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2026
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IF 10.4
Hongbo Li,Chen Li,Geng Long,Tian Su,Shuhua Zhang,Yang Zou,Xiaohong Chen,Hongjuan Li,Jinghua Yu
HA-SH-L-P is a novel redox-responsive hydrogel delivery system designed to enhance probiotic colonization, survival, and targeted delivery in the gastrointestinal tract through the synergistic interaction between l -glutamine and probiotics. This interaction not only improves probiotic viability but also modulates the immune microenvironment and strengthens intestinal barrier function. Using Limosilactobacillus fermentum CECT5716 as a model strain, the hydrogel demonstrated stable mechanical properties and responded to hydrogen sulfide (H₂S) in the intestinal microenvironment, enabling rapid probiotic release. In vitro, HA-SH-L-P significantly increased probiotic survival (by 3.56 log CFU/mL compared to free strains). In vivo, HA-SH-L-P modulated immune responses, maintained intestinal barrier integrity, and stabilized the gut microbiota. These results highlight the exceptional performance of HA-SH-L-P as a probiotic delivery system, offering a new approach for the treatment of related diseases.
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PubMed
高影响因子
ENVIRONMENTAL POLLUTION
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2022
·
IF 9.988
Caihong Wang,Zihong Pan,Yuanxiang Jin
Chlorinated polyfluorinated ether sulfonate (F–53 B) is a distinct substitute for perfluorooctane sulphonate. It has been reported to be biologically toxic to mammals, causing enteric toxicity, liver toxicity and neurotoxicity. However, studies about the effects of F–53 B on patients with gastrointestinal diseases such as inflammatory bowel disease are very limited. In this study, whether the toxic impacts of F–53 B on the gut and liver can be exacerbated in mice with colitis was explored. The sensitivity of mice with acute colitis caused by dextran sulfate sodium salt (DSS) to F–53 B was compared with that of healthy mice. The mice were administered water containing F–53 B at doses of 10 and 100 μg/L sequentially for two weeks, respectively. F–53 B exposure exacerbated DSS-induced colonic inflammation, including inducing shortening of colon length, inflammatory cell infiltration and more severe histopathological symptoms. In addition, F–53 B administration significantly increased the levels of inflammatory cytokines, including interleukin (IL)-1, IL-6 and tumour necrosis factor-α, in the plasma of mice with enteritis compared with control group. F–53 B impaired intestinal integrity of mice with colitis by downregulating Claudin-1 and antimicrobial peptide-related genes while elevating serum lipopolysaccharide levels. In addition, in mice with colitis, F–53 B increased the levels of serum total cholesterol, triglyceride, low-density lipoprotein cholesterol, aspartate aminotransferase, and alanine aminotransferase, resulted in more severe liver inflammation and increased the level of genes related to the Gasdermin D-mediated pyrolysis . Conclusively, our results indicated that F–53 B delayed the self-healing of ulcerative colitis (UC) and caused liver inflammation in mice. This study provided some new insights into the health risks of F–53 B and raises concerns about the health of individuals with UC.
研究领域:
毒理学
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胃肠病学
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免疫学
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肝病学
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产品关联
DOI
PubMed
高影响因子
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