PMID- 37647428
OWN - NLM
STAT- MEDLINE
DCOM- 20230901
LR  - 20230905
IS  - 2050-4527 (Electronic)
IS  - 2050-4527 (Linking)
VI  - 11
IP  - 8
DP  - 2023 Aug
TI  - Effects of N-acetyl-L-cysteine polysulfides on periodontitis in a mouse model.
PG  - e959
LID - 10.1002/iid3.959 [doi]
LID - e959
AB  - 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-1beta expression in bone 
      marrow-derived macrophages (BMDMs) could be inhibited by NAC-S2. On the other 
      hand, NAC-S2 suppressed the phosphorylation levels of IkappaB-alpha, p65, and IkappaB kinase 
      (IKK)-beta induced by LPS in BMDMs, while LPS induced phosphorylation of ERK1/2, 
      p38, and transforming growth factor beta-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-1beta, 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-kappaB pathway mediated 
      inflammation in mouse periodontitis model.
CI  - (c) 2023 The Authors. Immunity, Inflammation and Disease published by John Wiley & 
      Sons Ltd.
FAU - Sun, Xinxin
AU  - Sun X
AUID- ORCID: 0000-0001-7180-280X
AD  - Dental Department, Hejian Hospital of Traditional Chinese Medicine, Cangzhou 
      Central Hospital Medical Group, Cangzhou, Hebei, China.
FAU - Sun, Yaru
AU  - Sun Y
AD  - Dental Clinics, Cangzhou Central Hospital, Cangzhou, Hebei, China.
FAU - Cao, Sumin
AU  - Cao S
AD  - Dental Clinics, Cangzhou Central Hospital, Cangzhou, Hebei, China.
FAU - Liu, Xueli
AU  - Liu X
AD  - Dental Clinics, Cangzhou Central Hospital, Cangzhou, Hebei, China.
LA  - eng
PT  - Journal Article
PL  - England
TA  - Immun Inflamm Dis
JT  - Immunity, inflammation and disease
JID - 101635460
RN  - 9080-49-3 (polysulfide)
RN  - WYQ7N0BPYC (Acetylcysteine)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Toll-Like Receptor 4)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Animals
MH  - Mice
MH  - *Acetylcysteine/pharmacology
MH  - Lipopolysaccharides/toxicity
MH  - Toll-Like Receptor 4/genetics
MH  - *Periodontitis/drug therapy
MH  - Tumor Necrosis Factor-alpha
MH  - Disease Models, Animal
PMC - PMC10408371
OTO - NOTNLM
OT  - NAC-S2
OT  - NF-kappaB
OT  - TLR4
OT  - inflammation
OT  - periodontitis
COIS- The authors declare no conflict of interest.
EDAT- 2023/08/30 18:42
MHDA- 2023/09/01 06:43
PMCR- 2023/08/08
CRDT- 2023/08/30 14:13
PHST- 2023/07/10 00:00 [revised]
PHST- 2023/04/28 00:00 [received]
PHST- 2023/07/13 00:00 [accepted]
PHST- 2023/09/01 06:43 [medline]
PHST- 2023/08/30 18:42 [pubmed]
PHST- 2023/08/30 14:13 [entrez]
PHST- 2023/08/08 00:00 [pmc-release]
AID - IID3959 [pii]
AID - 10.1002/iid3.959 [doi]
PST - ppublish
SO  - Immun Inflamm Dis. 2023 Aug;11(8):e959. doi: 10.1002/iid3.959.