Ginsenoside Rh4 inhibits colorectal cancer via the modulation of gut microbiota-mediated bile acid metabolism DOI Creative Commons
Xue Bai, Zhiguang Duan, Jianjun Deng

et al.

Journal of Advanced Research, Journal Year: 2024, Volume and Issue: unknown

Published: July 1, 2024

Dysbiosis of the gut microbiota is emerging as a pivotal factor in pathogenesis colorectal cancer (CRC). Ginsenoside Rh4 (Rh4) an active compound isolated from ginseng with beneficial effects modulating intestinal inflammation and dysbiosis, but how regulates to alleviate CRC remains underexplored. We investigated impact on mechanism its action inhibiting via modulation microbiota. used AOM/DSS model employed transcriptomics, genomics metabolomics techniques explore inhibitory CRC. Furthermore, we experiments involving antibiotic treatment fecal transplantation (FMT) investigate role Finally, elucidated key functional bacteria metabolites regulated by Our research findings indicated that repaired barrier damage caused CRC, alleviated inflammation, inhibited development Additionally, microbiota-dependent manner. increased diversity microbiota, enriched probiotic Akkermansia muciniphila (A. muciniphila), dysbiosis Subsequently, A. muciniphila-mediated bile acid metabolism. promoted production UDCA enhancing activity 7α-hydroxysteroid dehydrogenase (7α-HSDH). further activated FXR, modulated TLR4-NF-κB signaling pathway, thus results confirm inhibits manner microbiota-mediated metabolism promoting UDCA, which activates FXR receptor pathway. has potential be modulator for preventing

Language: Английский

Microbiota–gut–brain axis: interplay between microbiota, barrier function and lymphatic system DOI Creative Commons

Miaomiao Zhuang,

Xun Zhang, Jun Cai

et al.

Gut Microbes, Journal Year: 2024, Volume and Issue: 16(1)

Published: Aug. 25, 2024

The human gastrointestinal tract, boasting the most diverse microbial community, harbors approximately 100 trillion microorganisms comprising viruses, bacteria, fungi, and archaea. profound genetic metabolic capabilities of gut microbiome underlie its involvement in nearly every facet biology, from health maintenance development to aging disease. Recent recognition microbiota – brain axis, referring bidirectional communication network between microbes their host, has led a surge interdisciplinary research. This review begins with an overview current understandings regarding influence on intestinal blood-brain barrier integrity. Subsequently, we discuss mechanisms examining role microbiota-related neural transmission, metabolites, hormones immunity. We propose concept microbiota-mediated multi-barrier modulation potential treatment neurological disorders. Furthermore, lymphatic function is discussed, providing insights into lesser-known conduits ecosystem within brain. In final section, conclude by describing ongoing frontiers understanding axis's impact

Language: Английский

Citations

11

Alleviative effects of exopolysaccharides from Limosilactobacillus mucosae CCFM1273 against ulcerative colitis via modulation of gut microbiota and inhibition of Fas/Fasl and TLR4/NF-κB pathways DOI
Huizhen Li, Haitao Li, Catherine Stanton

et al.

International Journal of Biological Macromolecules, Journal Year: 2024, Volume and Issue: 260, P. 129346 - 129346

Published: Jan. 21, 2024

Language: Английский

Citations

10

Fucoxanthin Alleviates Dextran Sulfate Sodium-Induced Colitis and Gut Microbiota Dysbiosis in Mice DOI

Yuhong Yang,

Chen Chen, Yan Zheng

et al.

Journal of Agricultural and Food Chemistry, Journal Year: 2024, Volume and Issue: 72(8), P. 4142 - 4154

Published: Feb. 14, 2024

The purpose of this study was to evaluate the preventive role and underlying mechanisms fucoxanthin (Fx) on dextran sulfate sodium (DSS)-induced colitis in mice. present data demonstrated that oral administration Fx (50 200 mg/kg body weight/day) for 36 days significantly alleviated severity DSS-treated mice, as evidenced by attenuating weight loss, bloody stool, diarrhea, shortened colon length, colonic epithelium distortion, a thin mucus layer, goblet cell depletion, damaged crypts, extensive infiltration inflammatory cells mucosa. Additionally, notably relieved DSS-induced intestinal epithelial barrier dysfunction via maintaining tight junction function preventing excessive apoptosis cells. Moreover, effectively diminished inflammation oxidative stress its might be due blunting activation NF-κB NLRP3 inflammasome signaling pathways. Furthermore, also modulates gut microbiota dysbiosis recovering richness diversity reshaping structure microbiota, such increasing

Language: Английский

Citations

10

Taurine Alleviates Experimental Colitis by Enhancing Intestinal Barrier Function and Inhibiting Inflammatory Response through TLR4/NF-κB Signaling DOI

Jiaming Zheng,

Jinglin Zhang, Yewen Zhou

et al.

Journal of Agricultural and Food Chemistry, Journal Year: 2024, Volume and Issue: 72(21), P. 12119 - 12129

Published: May 18, 2024

Taurine (Tau) is a semiessential amino acid in mammals with preventive and therapeutic effects on several intestinal disorders. However, the exact function of taurine ulcerative colitis (UC) still largely unclear. In this study, we used two taurine-deficient mouse models (CSAD–/– TauT–/– mice) to explore influence progression UC both dextran sulfate sodium (DSS)-induced LPS-stimulated Caco-2 cells. We found that cysteine sulfinic decarboxylase (CSAD) transporter (TauT) expressions levels were markedly reduced colonic tissues mice treated DSS. The CSAD TauT knockouts exacerbated DSS-induced clinical symptoms pathological damage aggravated barrier dysfunction mucosal inflammatory response. Conversely, pretreatment enhanced functions by increasing goblet cells upregulating tight junction protein expression. Importantly, bound TLR4 inhibited TLR4/NF-κB pathway, ultimately reducing proinflammatory factors (TNF-α IL-6) oxidative stress. Our findings highlight essential role maintaining integrity inhibiting inflammation, indicating promising supplement for treatment.

Language: Английский

Citations

10

Ginsenoside Rh4 inhibits colorectal cancer via the modulation of gut microbiota-mediated bile acid metabolism DOI Creative Commons
Xue Bai, Zhiguang Duan, Jianjun Deng

et al.

Journal of Advanced Research, Journal Year: 2024, Volume and Issue: unknown

Published: July 1, 2024

Dysbiosis of the gut microbiota is emerging as a pivotal factor in pathogenesis colorectal cancer (CRC). Ginsenoside Rh4 (Rh4) an active compound isolated from ginseng with beneficial effects modulating intestinal inflammation and dysbiosis, but how regulates to alleviate CRC remains underexplored. We investigated impact on mechanism its action inhibiting via modulation microbiota. used AOM/DSS model employed transcriptomics, genomics metabolomics techniques explore inhibitory CRC. Furthermore, we experiments involving antibiotic treatment fecal transplantation (FMT) investigate role Finally, elucidated key functional bacteria metabolites regulated by Our research findings indicated that repaired barrier damage caused CRC, alleviated inflammation, inhibited development Additionally, microbiota-dependent manner. increased diversity microbiota, enriched probiotic Akkermansia muciniphila (A. muciniphila), dysbiosis Subsequently, A. muciniphila-mediated bile acid metabolism. promoted production UDCA enhancing activity 7α-hydroxysteroid dehydrogenase (7α-HSDH). further activated FXR, modulated TLR4-NF-κB signaling pathway, thus results confirm inhibits manner microbiota-mediated metabolism promoting UDCA, which activates FXR receptor pathway. has potential be modulator for preventing

Language: Английский

Citations

10