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Effects of N‐acetyl‐L‐cysteine polysulfides on periodontitis in a mouse model

BACKGROUND: Polysulfides are reported to be involved in various important biological processes. N‐acetyl‐l‐cysteine polysulfide with 2 sulfane sulfur atoms (NAC‐S2) regulates diverse toll‐like receptor (TLR) signaling pathways. Here, we aimed to determine the role of NAC‐S2 in periodontitis and expl...

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Autores principales: Sun, Xinxin, Sun, Yaru, Cao, Sumin, Liu, Xueli
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10408371/
https://www.ncbi.nlm.nih.gov/pubmed/37647428
http://dx.doi.org/10.1002/iid3.959
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author Sun, Xinxin
Sun, Yaru
Cao, Sumin
Liu, Xueli
author_facet Sun, Xinxin
Sun, Yaru
Cao, Sumin
Liu, Xueli
author_sort Sun, Xinxin
collection PubMed
description BACKGROUND: Polysulfides are reported to be involved in various important biological processes. N‐acetyl‐l‐cysteine polysulfide with 2 sulfane sulfur atoms (NAC‐S2) regulates diverse toll‐like receptor (TLR) signaling pathways. Here, we aimed to determine the role of NAC‐S2 in periodontitis and explore the potential mechanism. METHODS: A periodontitis mouse model was established by ligating the subgingival between the first and second molars in wild‐type, TLR4(‐/‐), and Myd88(‐/‐) mice. RESULTS: NAC‐S2 did not affect the proportion of macrophages (CD11b(+)F4/80(+)) or neutrophils (CD11b(+)GR‐1(+)) in the bone marrow. Mechanically, lipopolysaccharides (LPS), Zymosan A, or poly I: C induced tumor necrosis factor (TNF), interleukin (IL)‐6, and IL‐1β expression in bone marrow‐derived macrophages (BMDMs) could be inhibited by NAC‐S2. On the other hand, NAC‐S2 suppressed the phosphorylation levels of IκB‐α, p65, and IκB kinase (IKK)‐β induced by LPS in BMDMs, while LPS induced phosphorylation of ERK1/2, p38, and transforming growth factor β‐activated kinase 1 (TAK1) could not be affected by NAC‐S2. In wild‐type periodontitis mice, NAC‐S2 administration decreased the cemento‐enamel‐junction–alveolar bone crest (CEJ‐ABC) distance and the relative mRNA expression of TNF, IL‐6, and IL‐1β, while such phenomena could not be observed in TLR4 deficiency or Myd88 deficiency mice. CONCLUSIONS: All of these results indicate that NAC‐S2 ameliorates TLR4/NF‐κB pathway mediated inflammation in mouse periodontitis model.
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spelling pubmed-104083712023-08-09 Effects of N‐acetyl‐L‐cysteine polysulfides on periodontitis in a mouse model Sun, Xinxin Sun, Yaru Cao, Sumin Liu, Xueli Immun Inflamm Dis Original Articles BACKGROUND: Polysulfides are reported to be involved in various important biological processes. N‐acetyl‐l‐cysteine polysulfide with 2 sulfane sulfur atoms (NAC‐S2) regulates diverse toll‐like receptor (TLR) signaling pathways. Here, we aimed to determine the role of NAC‐S2 in periodontitis and explore the potential mechanism. METHODS: A periodontitis mouse model was established by ligating the subgingival between the first and second molars in wild‐type, TLR4(‐/‐), and Myd88(‐/‐) mice. RESULTS: NAC‐S2 did not affect the proportion of macrophages (CD11b(+)F4/80(+)) or neutrophils (CD11b(+)GR‐1(+)) in the bone marrow. Mechanically, lipopolysaccharides (LPS), Zymosan A, or poly I: C induced tumor necrosis factor (TNF), interleukin (IL)‐6, and IL‐1β expression in bone marrow‐derived macrophages (BMDMs) could be inhibited by NAC‐S2. On the other hand, NAC‐S2 suppressed the phosphorylation levels of IκB‐α, p65, and IκB kinase (IKK)‐β induced by LPS in BMDMs, while LPS induced phosphorylation of ERK1/2, p38, and transforming growth factor β‐activated kinase 1 (TAK1) could not be affected by NAC‐S2. In wild‐type periodontitis mice, NAC‐S2 administration decreased the cemento‐enamel‐junction–alveolar bone crest (CEJ‐ABC) distance and the relative mRNA expression of TNF, IL‐6, and IL‐1β, while such phenomena could not be observed in TLR4 deficiency or Myd88 deficiency mice. CONCLUSIONS: All of these results indicate that NAC‐S2 ameliorates TLR4/NF‐κB pathway mediated inflammation in mouse periodontitis model. John Wiley and Sons Inc. 2023-08-08 /pmc/articles/PMC10408371/ /pubmed/37647428 http://dx.doi.org/10.1002/iid3.959 Text en © 2023 The Authors. Immunity, Inflammation and Disease published by John Wiley & Sons Ltd. https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Articles
Sun, Xinxin
Sun, Yaru
Cao, Sumin
Liu, Xueli
Effects of N‐acetyl‐L‐cysteine polysulfides on periodontitis in a mouse model
title Effects of N‐acetyl‐L‐cysteine polysulfides on periodontitis in a mouse model
title_full Effects of N‐acetyl‐L‐cysteine polysulfides on periodontitis in a mouse model
title_fullStr Effects of N‐acetyl‐L‐cysteine polysulfides on periodontitis in a mouse model
title_full_unstemmed Effects of N‐acetyl‐L‐cysteine polysulfides on periodontitis in a mouse model
title_short Effects of N‐acetyl‐L‐cysteine polysulfides on periodontitis in a mouse model
title_sort effects of n‐acetyl‐l‐cysteine polysulfides on periodontitis in a mouse model
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10408371/
https://www.ncbi.nlm.nih.gov/pubmed/37647428
http://dx.doi.org/10.1002/iid3.959
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