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Hydrogen sulfide attenuates TMAO‑induced macrophage inflammation through increased SIRT1 sulfhydration

  • Authors:
    • Mi-Hua Liu
    • Xiao-Long Lin
    • Le-Le Xiao
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    Affiliations: Department of Clinical Laboratory, The Affiliated Ganzhou Hospital of Nanchang University, Ganzhou, Jiangxi 341000, P.R. China, Department of Pathology, Huizhou Third People's Hospital, Guangzhou Medical University, Huizhou, Guangdong 516002, P.R. China, Intensive Care Unit, The Affiliated Ganzhou Hospital of Nanchang University, Ganzhou, Jiangxi 341000, P.R. China
    Copyright: © Liu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Article Number: 129
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    Published online on: May 16, 2023
       https://doi.org/10.3892/mmr.2023.13016
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Abstract

Chronic inflammation is a key factor that accelerates the progression of inflammatory vascular disease. Hydrogen sulfide (H2S) has potent anti‑inflammatory effects; however, its underlying mechanism of action has not been fully elucidated. The present study aimed to investigate the potential effect of H2S on sirtuin 1 (SIRT1) sulfhydration in trimethylamine N‑oxide (TMAO)‑induced macrophage inflammation, and its underlying mechanism. Pro‑inflammatory M1 cytokines (MCP‑1, IL‑1β, and IL‑6) and anti‑inflammatory M2 cytokines (IL‑4 and IL‑10) were detected by RT‑qPCR. CSE, p65 NF‑κB, p‑p65 NF‑κB, IL‑1β, IL‑6 and TNF‑α levels were measured by Western blot. The results revealed that cystathionine γ‑lyase protein expression was negatively associated with TMAO‑induced inflammation. Sodium hydrosulfide (a donor of H2S) increased SIRT1 expression and inhibited the expression of inflammatory cytokines in TMAO‑stimulated macrophages. Furthermore, nicotinamide, a SIRT1 inhibitor, antagonized the protective effect of H2S, which contributed to P65 NF‑κB phosphorylation and upregulated the expression of inflammatory factors in macrophages. H2S ameliorated TMAO‑induced activation of the NF‑κB signaling pathway via SIRT1 sulfhydration. Moreover, the antagonistic effect of H2S on inflammatory activation was largely eliminated by the desulfhydration reagent dithiothreitol. These results indicated that H2S may prevent TMAO‑induced macrophage inflammation by reducing P65 NF‑κB phosphorylation via the upregulation and sulfhydration of SIRT1, suggesting that H2S may be used to treat inflammatory vascular diseases.
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Spandidos Publications style
Liu M, Lin X and Xiao L: Hydrogen sulfide attenuates TMAO‑induced macrophage inflammation through increased SIRT1 sulfhydration. Mol Med Rep 28: 129, 2023.
APA
Liu, M., Lin, X., & Xiao, L. (2023). Hydrogen sulfide attenuates TMAO‑induced macrophage inflammation through increased SIRT1 sulfhydration. Molecular Medicine Reports, 28, 129. https://doi.org/10.3892/mmr.2023.13016
MLA
Liu, M., Lin, X., Xiao, L."Hydrogen sulfide attenuates TMAO‑induced macrophage inflammation through increased SIRT1 sulfhydration". Molecular Medicine Reports 28.1 (2023): 129.
Chicago
Liu, M., Lin, X., Xiao, L."Hydrogen sulfide attenuates TMAO‑induced macrophage inflammation through increased SIRT1 sulfhydration". Molecular Medicine Reports 28, no. 1 (2023): 129. https://doi.org/10.3892/mmr.2023.13016
Copy and paste a formatted citation
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Spandidos Publications style
Liu M, Lin X and Xiao L: Hydrogen sulfide attenuates TMAO‑induced macrophage inflammation through increased SIRT1 sulfhydration. Mol Med Rep 28: 129, 2023.
APA
Liu, M., Lin, X., & Xiao, L. (2023). Hydrogen sulfide attenuates TMAO‑induced macrophage inflammation through increased SIRT1 sulfhydration. Molecular Medicine Reports, 28, 129. https://doi.org/10.3892/mmr.2023.13016
MLA
Liu, M., Lin, X., Xiao, L."Hydrogen sulfide attenuates TMAO‑induced macrophage inflammation through increased SIRT1 sulfhydration". Molecular Medicine Reports 28.1 (2023): 129.
Chicago
Liu, M., Lin, X., Xiao, L."Hydrogen sulfide attenuates TMAO‑induced macrophage inflammation through increased SIRT1 sulfhydration". Molecular Medicine Reports 28, no. 1 (2023): 129. https://doi.org/10.3892/mmr.2023.13016
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