Effects of N‐acetyl‐L‐cysteine polysulfides on periodontitis in a mouse model
Abstract 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...
| Main Authors: | , , , |
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| Format: | Article |
| Language: | English |
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Wiley
2023-08-01
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| Series: | Immunity, Inflammation and Disease |
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| Online Access: | https://doi.org/10.1002/iid3.959 |
| _version_ | 1797645439927844864 |
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| author | Xinxin Sun Yaru Sun Sumin Cao Xueli Liu |
| author_facet | Xinxin Sun Yaru Sun Sumin Cao Xueli Liu |
| author_sort | Xinxin Sun |
| collection | DOAJ |
| description | Abstract 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. |
| first_indexed | 2024-03-11T14:46:23Z |
| format | Article |
| id | doaj.art-8831cc2f148f4fcebd085285f2d59456 |
| institution | Directory Open Access Journal |
| issn | 2050-4527 |
| language | English |
| last_indexed | 2024-03-11T14:46:23Z |
| publishDate | 2023-08-01 |
| publisher | Wiley |
| record_format | Article |
| series | Immunity, Inflammation and Disease |
| spelling | doaj.art-8831cc2f148f4fcebd085285f2d594562023-10-30T10:50:33ZengWileyImmunity, Inflammation and Disease2050-45272023-08-01118n/an/a10.1002/iid3.959Effects of N‐acetyl‐L‐cysteine polysulfides on periodontitis in a mouse modelXinxin Sun0Yaru Sun1Sumin Cao2Xueli Liu3Dental Department, Hejian Hospital of Traditional Chinese Medicine Cangzhou Central Hospital Medical Group Cangzhou Hebei ChinaDental Clinics Cangzhou Central Hospital Cangzhou Hebei ChinaDental Clinics Cangzhou Central Hospital Cangzhou Hebei ChinaDental Clinics Cangzhou Central Hospital Cangzhou Hebei ChinaAbstract 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.https://doi.org/10.1002/iid3.959inflammationNAC‐S2NF‐κBperiodontitisTLR4 |
| spellingShingle | Xinxin Sun Yaru Sun Sumin Cao Xueli Liu Effects of N‐acetyl‐L‐cysteine polysulfides on periodontitis in a mouse model Immunity, Inflammation and Disease inflammation NAC‐S2 NF‐κB periodontitis TLR4 |
| 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 | inflammation NAC‐S2 NF‐κB periodontitis TLR4 |
| url | https://doi.org/10.1002/iid3.959 |
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