BMC GASTROENTEROLOGY
·
2025
·Vol. 25
·期 1
·1-17
·
IF 2.6
Lv Jie,Chen Qianqian,Yang Lu,Guan Jing,Wang Sheng,Gui Gen,Yang Zhaoyun,Wang Xu,Sun Bin
IntroductionThe incidence of colorectal cancer (CRC) is increasing with colorectal adenomas recognized as key precancerous lesions. Emerging evidence suggests that Imidazole propionate (ImP), a metabolite of gut microbiota, is elevated in patients, indicating a potential role in tumorigenesis of CRC.ObjectivesThis study aimed to validate a novel method for detecting serum ImP using 3-piperazin-1-yl-propionic acid as an internal standard (IS), and to compare ImP levels between patients with colorectal adenomas and colorectal cancer.Methods Serum ImP were measured using Ultra-Performance Liquid Chromatography Tandem Mass Spectrometry (UPLC-MS/MS) with 3-piperazin-1-yl-propionic acid as the IS. Four distinct patient groups were analyzed.Results The use of 3-piperazin-1-yl-propionic acid as an IS was successfully validated for the quantification of ImP. Serum ImP differed significantly among the groups, showing a stepwise increase from healthy controls to patients with colorectal adenomas and CRC. Notably, ImP concentrations were significantly higher in CRC patients than in other groups.Conclusion This study demonstrates the successful application of 3-piperazin-1-yl-propionic acid as an IS provides a viable method for measuring serum ImP concentrations. The results suggest a potential link between ImP and colorectal cancer development.
研究领域:
医学
·
肿瘤学
·
微生物组学
·
代谢组学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
MOLECULAR MEDICINE
·
2025
·Vol. 31
·期 1
·1-14
·
IF 6.4
Jin Shengkai,Zhou Yuhua,Lv Jing,Lu Yichen,Zhang Yuwei,Li Menglu,Feng Ninghan
Background A close relationship exists between castration-resistant prostate cancer (CRPC) and histidine metabolism by gut microbes. However, the effects of the histidine metabolite imidazole propionate (IMP) on prostate cancer (PCa) and its underlying mechanisms are not well understood.Methods We first assessed the effects of IMP on cell proliferation and migration at the cellular level. Subsequently, we investigated the mechanism of action of IMP using transcriptome sequencing, qPCR, and Western blot analysis. Finally, we validated our findings in vivo using a mouse model.Results Histidine had no effect on PCa cell proliferation; however, IMP significantly inhibited the proliferation and migration of PC3 and DU145 cells. Mechanistic studies indicate that IMP exerts its effects by upregulating PDZK1 expression, which subsequently inhibits the phosphorylation of the PI3K-AKT pathway.Conclusion sIn conclusion, IMP significantly inhibits the progression of PCa, offering new insights into potential treatments for CRPC.
研究领域:
肿瘤学
·
微生物学
·
分子生物学
·
癌症研究
✓ 已验证
产品关联
DOI
PubMed
高影响因子
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
·
2021
·Vol. 22
·期 21
·11436
·
IF 5.924
Zhiyuan Chen,Bin Wang,Jiali Dong,Yuan Li,Shuqin Zhang,Xiaozhou Zeng,Huiwen Xiao,Saijun Fan,Ming Cui
Radiation-induced cardiopulmonary injuries are the most common and intractable side effects that are entwined with radiotherapy for thorax cancers. However, the therapeutic options for such complications have yielded disappointing results in clinical applications. Here, we reported that gut microbiota-derivedl-Histidine and its secondary metabolite imidazole propionate (ImP) fought against radiation-induced cardiopulmonary injury in an entiric flora-dependent manner in mouse models. Local chest irradiation decreased the level ofl-Histidine in fecal pellets, which was increased following fecal microbiota transplantation.l-Histidine replenishment via an oral route retarded the pathological process of lung and heart tissues and improved lung respiratory and heart systolic function following radiation exposure.l-Histidine preserved the gut bacterial taxonomic proportions shifted by total chest irradiation but failed to perform radioprotection in gut microbiota-deleted mice. ImP, the downstream metabolite ofl-Histidine, accumulated in peripheral blood and lung tissues followingl-Histidine replenishment and protected against radiation-induced lung and heart toxicity. Orally gavaged ImP could not enter into the circulatory system in mice through an antibiotic cocktail treatment. Importantly, ImP inhibited pyroptosis to nudge lung cell proliferation after radiation challenge. Together, our findings pave a novel method of protection against cardiopulmonary complications intertwined with radiotherapy in pre-clinical settings and underpin the idea that gut microbiota-producedl-Histidine and ImP are promising radioprotective agents.Keywords:radiation-induced cardiopulmonary injury;gut microbiota metabolites;imidazole propionate;pyroptosis;l-histidine
研究领域:
肿瘤学
·
药理学
·
微生物学
·
心血管科学
·
肺科学
✓ 已验证
DOI
PubMed
高影响因子
PHYTOTHERAPY RESEARCH
·
2025
·
IF 6.3
Jingyi Hu,Feng Xu,Lei Zhu,Yuan Cui,Ryan Au,Yanan Li,Yiheng Tong,Hong Shen
Angelica dahurica radix (ADR), the root of the botanical family Apiaceae (genus Angelica , species Angelica dahurica ( Hoffm .)), has been used to treat colitis in clinical practice. The immunomodulatory effects of ADR are attributed to its polysaccharides (RP). However, its mechanism of action has not been elucidated. In this study, RP's structure was determined through nuclear magnetic resonance analysis. Dextran sulfate sodium-induced colitis in mice was utilized to assess the therapeutic efficacy of RP, while experiments involving fecal microbiota transplantation (FMT) and antibiotic treatment were performed to investigate the contribution of gut microbiota to RP's protective function. Non-targeted metabolomics was utilized to identify potential targets for elucidating the underlying mechanisms. RP is likely composed of (→4)-α-D-Glcp-(1→ and →4)-α-D-Galp-(1→). It effectively alleviated DSS-induced colitis by restoring the balance of the gut microbial community, a finding validated through FMT and antibiotic intervention experiments. Imidazole propionate (ImP) emerged as a potential target for RP's efficacy in treating colitis, which inhibits the activation of peroxisome proliferator-activated receptor gamma (PPAR-γ). Our findings suggest that RP may confer protection against colitis by activating the PPAR-γ signaling pathway through alleviating the constraint imposed by ImP.
研究领域:
药理学
·
微生物学
·
免疫学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
危险品化学品经营许可证（带存储）