Urolithin A attenuates arsenic-induced gut barrier dysfunction

Ghosh, Sweta; Banerjee, Minakshi; Haribabu, Bodduluri; Jala, Venkatakrishna R.

doi:10.1007/s00204-022-03232-2

Cited by 16 publications

(18 citation statements)

References 107 publications

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“…55 UA was also found to prevent inorganic arsenic-induced disruption of tight junctional proteins in intestinal epithelial cells by blocking oxidative stress and markers of inflammation. 85 Our study showed that UA could reverse the low expression of Ocln and Zo1 caused by H. pylori (Figure 7), which were consistent with the conclusion. The risk of developing severe diseases by H. pylori infection is determined by the expression of its virulence factors.…”

Section: ■ Discussionsupporting

confidence: 90%

“…It has been demonstrated that UA significantly enhanced the gut barrier function through the up-regulation of the epithelial tight junctions’ proteins . UA was also found to prevent inorganic arsenic-induced disruption of tight junctional proteins in intestinal epithelial cells by blocking oxidative stress and markers of inflammation . Our study showed that UA could reverse the low expression of Ocln and Zo1 caused by H.…”

Section: Discussionsupporting

confidence: 52%

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Urolithin A Attenuates Helicobacter pylori-Induced Damage In Vivo

Cao

Wang

et al. 2022

J. Agric. Food Chem.

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Urolithin A (UA) is a metabolite produced in the gut following the consumption of ellagic acid (EA) rich foods. EA has shown anti-inflammatory, antioxidant, and anticancer properties. Because EA is poorly absorbed in the gastrointestinal tract, urolithins are considered to play a major role in bioactivity. Helicobacter pylori (H. pylori) infection is the most common chronic bacterial infection all over the world. It is potentially hazardous to humans because of its relationship to various gastrointestinal diseases. In this study, we investigated the effect of UA on inflammation by H. pylori. The results indicated that UA attenuated H. pylori-induced inflammation in vitro and in vivo. UA also reduced the secretion of H. pylori virulence factors and tissue injuries in mice. Furthermore, UA decreased the relative abundance of Helicobacteraceae in feces of H. pylori-infected mice. In summary, taking UA effectively inhibited the injury caused by H. pylori.

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Section: ■ Discussionsupporting

confidence: 90%

Section: Discussionsupporting

confidence: 52%

Urolithin A Attenuates Helicobacter pylori-Induced Damage In Vivo

Cao

Wang

et al. 2022

J. Agric. Food Chem.

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“…Total RNA was prepared from colon tissues of WT and Cyp1a1 −/− mice using Maxwell ® 16 LEV simplyRNA tissue kits (Promega) and changes in expression of ZO-1, Occludin and Cldn4 genes were analyzed as previously described ( 9 , 11 , 26 ). Fold changes in gene expression levels were calculated using the 2 -ΔΔ CT method using β-actin as a housekeeping gene control and normalized to the untreated control of each mice group.…”

Section: Methodsmentioning

confidence: 99%

“…Urolithin A (UroA) is a microbial metabolite derived from polyphenolic compounds such as ellagitannins (ETs) and ellagic acid (EA) of berries and pomegranates. Urolithin A has been shown to render numerous health benefits by mediating antioxidative, anti-inflammatory, anti-diabetic, anti-cancer and anti-ageing effects (8)(9)(10)(11). Previously, our group demonstrated that UroA enhanced gut barrier function through upregulating junctional proteins and reducing unwarranted inflammation through activation of aryl hydrocarbon receptor (AhR)-nuclear factor erythroid 2-related factor 2 (Nrf2)-dependent pathways (11).…”

Section: Introductionmentioning

confidence: 99%

Cytochrome P450 1A1 is essential for the microbial metabolite, Urolithin A-mediated protection against colitis

et al. 2022

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BackgroundCytochrome P450 Family 1 Subfamily A Member 1 (CYP1A1) pathway, which is regulated by aryl hydrocarbon receptor (AhR) plays an important role in chemical carcinogenesis and xenobiotic metabolism. Recently, we demonstrated that the microbial metabolite Urolithin A (UroA) mitigates colitis through its gut barrier protective and anti-inflammatory activities in an AhR-dependent manner. Here, we explored role of CYP1A1 in UroA-mediated gut barrier and immune functions in regulation of inflammatory bowel disease (IBD).MethodsTo determine the role of CYP1A1 in UroA-mediated protectives activities against colitis, we subjected C57BL/6 mice and Cyp1a1-/- mice to dextran sodium sulphate (DSS)-induced acute colitis model. The phenotypes of the mice were characterized by determining loss of body weight, intestinal permeability, systemic and colonic inflammation. Further, we evaluated the impact of UroA on regulation of immune cell populations by flow cytometry and confocal imaging using both in vivo and ex vivo model systems.ResultsUroA treatment mitigated DSS-induced acute colitis in the wildtype mice. However, UroA-failed to protect Cyp1a1-/- mice against colitis, as evident from non-recovery of body weight loss, shortened colon lengths and colon weight/length ratios. Further, UroA failed to reduce DSS-induced inflammation, intestinal permeability and upregulate tight junction proteins in Cyp1a1-/- mice. Interestingly, UroA induced the expansion of T-reg cells in a CYP1A1-dependent manner both in vivo and ex vivo models.ConclusionOur results suggest that CYP1A1 expression is essential for UroA-mediated enhanced gut barrier functions and protective activities against colitis. We postulate that CYP1A1 plays critical and yet unknown functions beyond xenobiotic metabolism in the regulation of gut epithelial integrity and immune systems to maintain gut homeostasis in IBD pathogenesis.

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“…Similarly, urolithin-A ameliorated cytokine-induced inflammation in human colon fibroblasts via downregulation of the levels of IL-8 and phenyl glycidyl ether E2 (PGE 2 ), as well as cell migration and adhesion [164]. Some studies also revealed the protective effects of urolithin-A on gut barrier integrity [165,166]. Taken together, whether the intestinal inflammatory effects of EA are due to its microbiota-derived urolithins requires further characterization.…”

Section: Ellagic Acid (Ea)mentioning

confidence: 99%

Pharmacological Effects of Polyphenol Phytochemicals on the Intestinal Inflammation via Targeting TLR4/NF-κB Signaling Pathway

Wang

Yang

2022

IJMS

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TLR4/NF-κB is a key inflammatory signaling transduction pathway, closely involved in cell differentiation, proliferation, apoptosis, and pro-inflammatory response. Toll like receptor 4 (TLR4), the first mammalian TLR to be characterized, is the innate immune receptor that plays a key role in inflammatory signal transductions. Nuclear factor kappa B (NF-κB), the TLR4 downstream, is the key to accounting for the expression of multiple genes involved in inflammatory responses, such as pro-inflammatory cytokines. Inflammatory bowel disease (IBD) in humans is a chronic inflammatory disease with high incidence and prevalence worldwide. Targeting the TLR4/NF-κB signaling pathway might be an effective strategy to alleviate intestinal inflammation. Polyphenol phytochemicals have shown noticeable alleviative effects by acting on the TLR4/NF-κB signaling pathway in intestinal inflammation. This review summarizes the pharmacological effects of more than 20 kinds of polyphenols on intestinal inflammation via targeting the TLR4/NF-κB signaling pathway. We expected that polyphenol phytochemicals targeting the TLR4/NF-κB signaling pathway might be an effective approach to treat IBD in future clinical research applications.

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Urolithin A attenuates arsenic-induced gut barrier dysfunction

Cited by 16 publications

References 107 publications

Urolithin A Attenuates Helicobacter pylori-Induced Damage In Vivo

Urolithin A Attenuates Helicobacter pylori-Induced Damage In Vivo

Cytochrome P450 1A1 is essential for the microbial metabolite, Urolithin A-mediated protection against colitis

Pharmacological Effects of Polyphenol Phytochemicals on the Intestinal Inflammation via Targeting TLR4/NF-κB Signaling Pathway

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