Arsenic trioxide ameliorates murine colon inflammation through inflammatory cell enzymatic modulation

Moulahoum, Hichem; Boumaza, Belkacem Mohamed Amine; Ferrat, Meriem; Bounaama, Abdelkader; Djerdjouri, Bahia

doi:10.1007/s00210-018-1578-1

Naunyn-Schmiedeberg's Arch Pharmacol

2018

DOI: 10.1007/s00210-018-1578-1

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Arsenic trioxide ameliorates murine colon inflammation through inflammatory cell enzymatic modulation

Hichem Moulahoum

Belkacem Mohamed Amine Boumaza

Meriem Ferrat

et al.

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Cited by 6 publications

(1 citation statement)

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“…Excessive uncontrolled inflammatory responses can result in dysregulation of immunological homeostasis, followed by a variety of inflammatory diseases. While inflammatory response is recently recognized as one of the major mechanisms for many inflammatory diseases, including inflammatory bowel diseases (IBDs) and hypersensitivities [9, 21, 30], it still remains unknown how inflammatory response through several organs affects the homeostasis of the living organism. The pathogenesis of inflammatory diseases is characterized by an imbalanced activation of inflammatory and anti-inflammatory response (Fig.…”

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The clarified role of interleukin-19 in the inflammatory bowel disease and hypersensitivity: Insights from animal models and humans

Fujimoto

Aono

Azuma

2019

The Journal of Veterinary Medical Science

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The cytokine interleukin-19 (IL-19) is a member of the IL-10 family that includes IL-20, IL-22, IL-24, and IL-26. Previous studies indicated that IL-19 is produced by keratinocytes, epithelial cells, macrophages, and B-cells. Especially, the number of IL-4-producing T cells increased, whereas the number of IFN-γ-producing T cells decreased when naive T cells from healthy people were cultured in the presence of IL-19. There is an increasing body of data demonstrating that IL-19 is associated with the development of type 1 helper T cell-responses, although IL-19 was originally associated with the development of type 2 helper T cell-responses. In this review, we will attempt to discuss current knowledge about the role of IL-19 on several T cell response-mediated inflammatory diseases including inflammatory bowel disease and hypersensitivity.

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mentioning

confidence: 99%

The clarified role of interleukin-19 in the inflammatory bowel disease and hypersensitivity: Insights from animal models and humans

Fujimoto

Aono

Azuma

2019

The Journal of Veterinary Medical Science

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Ferulic Acid Inhibits Arsenic‐Induced Colon Injury by Improving Intestinal Barrier Function

Wang,

Hong,

et al. 2024

Environmental Toxicology

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The prolonged exposure to arsenic results in intestinal barrier dysfunction, which is strongly concerned with detrimental processes such as oxidative stress and the inflammatory response. Ferulic acid (FA), as a phenolic acid, possesses the capability to mitigate arsenic‐induced liver damage and cardiotoxic effects dependent on inhibition of oxidative stress and inflammatory responses. FA can mitigate testicular tissue damage and alveolar epithelial dysfunction, the mechanism of which may rely on nuclear factor erythroid 2‐related factor 2/heme oxygenase 1 (Nrf2/HO‐1) activation and nuclear factor‐kappa B (NF‐κB) pathway blocking. Based on the antioxidant and anti‐inflammatory properties of FA, we speculated that FA might have the potential to inhibit arsenic‐induced intestinal damage. To confirm this scientific hypothesis, mice exposed to sodium arsenite were treated with FA to observe colonic histopathology and TJ protein levels, and oxidative stress and TJ protein levels in Caco‐2 cells exposed to sodium arsenite were assessed after FA intervention. In addition, molecular levels of NF‐κB and Nrf2/HO‐1 pathway in colon and Caco‐2 cells were also detected. As shown in our data, FA inhibited arsenic‐induced colon injury, which was reflected in the improvement of mucosal integrity, the decrease of down‐regulated expression of tight junction (TJ) proteins (Claudin‐1, Occludin, and ZO‐1) and the inhibition of oxidative stress. Similarly, treatment with FA attenuated the inhibitory effect of arsenic on TJ protein expression in Caco‐2 cells. In addition to suppressing the activation of NF‐κB pathway, FA retrieved the activation of Nrf2/HO‐1 pathway in colon and intestinal epithelial cells induced by arsenic. In summary, our findings propose that FA has the potential to mitigate arsenic‐induced intestinal damage by preserving the integrity of intestinal epithelial TJs and suppressing oxidative stress. These results lay the groundwork for the potential use of FA in treating colon injuries caused by arsenic.

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Identifying Hub Genes, Key Pathways and Immune Cell Infiltration Characteristics in Pediatric and Adult Ulcerative Colitis by Integrated Bioinformatic Analysis

et al. 2020

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Arsenic trioxide ameliorates murine colon inflammation through inflammatory cell enzymatic modulation

Cited by 6 publications

References 53 publications

The clarified role of interleukin-19 in the inflammatory bowel disease and hypersensitivity: Insights from animal models and humans

The clarified role of interleukin-19 in the inflammatory bowel disease and hypersensitivity: Insights from animal models and humans

Ferulic Acid Inhibits Arsenic‐Induced Colon Injury by Improving Intestinal Barrier Function

Identifying Hub Genes, Key Pathways and Immune Cell Infiltration Characteristics in Pediatric and Adult Ulcerative Colitis by Integrated Bioinformatic Analysis

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