Evidence map›Paper›PMID 32945495›Full record

ArticleMolecular medicine reports2020

N‑acetyl cysteine inhibits the lipopolysaccharide‑induced inflammatory response in bone marrow mesenchymal stem cells by suppressing the TXNIP/NLRP3/IL‑1β signaling pathway.

Xuemei Wang, Mengyi Jiang, Xiaoping He, Bo Zhang, Wei Peng, Ling Guo

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.0field-weighted citation impact, top 25% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

20 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Pyroptosis in bone loss.Apoptosis : an international journal on programmed cell death · 2023
    Review
  13. Article
  14. Article
  15. Article
  16. S14G-humanin (HNG) protects retinal endothelial cells from UV-B-induced NLRP3 inflammation activation through inhibiting Egr-1.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2021
    Article
  17. Article
  18. S1P/S1PAntioxidants (Basel, Switzerland) · 2021
    Article
  19. Review
  20. Inflammasomes in Alveolar Bone Loss.Frontiers in immunology · 2021
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Xuemei WangDepartment of Prosthodontics, Hospital of Stomatology Affiliated to Southwest Medical University, Luzhou, Sichuan 646000, P.R. China.
Mengyi JiangDepartment of Prosthodontics, Hospital of Stomatology Affiliated to Southwest Medical University, Luzhou, Sichuan 646000, P.R. China.
Xiaoping HeDepartment of Prosthodontics, Hospital of Stomatology Affiliated to Southwest Medical University, Luzhou, Sichuan 646000, P.R. China.
Bo ZhangDepartment of Prosthodontics, Hospital of Stomatology Affiliated to Southwest Medical University, Luzhou, Sichuan 646000, P.R. China.
Wei PengDepartment of Prosthodontics, Hospital of Stomatology Affiliated to Southwest Medical University, Luzhou, Sichuan 646000, P.R. China.
Ling GuoDepartment of Prosthodontics, Hospital of Stomatology Affiliated to Southwest Medical University, Luzhou, Sichuan 646000, P.R. China.
Southwest Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

N-acetyl cysteine (NAC) has been used to inhibit lipopolysaccharide (LPS)-induced inflammation. However, the molecular mechanism underlying its anti‑inflammatory effects remains to be elucidated. The present study aimed to determine the effect of NAC on the LPS‑induced inflammatory response in bone marrow mesenchymal stem cells (BMSCs) and elucidate the underlying molecular mechanism. First, BMSCs were stimulated by LPS following pretreatment with NAC (0, 0.1, 0.5, 1 or 2 mM). A Cell Counting Kit 8 assay was used to determine the number of viable cells and 1 mM NAC was selected as the experimental concentration. Then, the secretion of inflammatory factors, including interleukin (IL)‑1β, IL‑6 and tumor necrosis factor‑α was evaluated by enzyme‑linked immunosorbent assay. Finally, the expression levels of mRNA and proteins, including apoptosis‑associated speck‑like protein containing a CARD (ASC), nucleotide‑binding oligomerization domain‑like receptor protein 3 (NLRP3), caspase‑1, thioredoxin‑interacting protein (TXNIP), and thioredoxin (TRX), were evaluated by reverse transcription‑quantitative PCR and western blot analysis, respectively. The results demonstrated that the secretion of inflammatory factors, which was increased by the administration of LPS, was reduced by pretreatment with NAC. Furthermore, NAC reduced the expression of ASC, NLRP3, caspase‑1 and TXNIP, but enhanced that of TRX. To conclude, NAC had anti‑inflammatory effects on LPS‑stimulated BMSCs, which was closely associated with the TXNIP/NLRP3/IL‑1β signaling pathway. Thus, NAC may be a promising treatment to attenuate the inflammatory response in LPS‑induced BMSCs.

Indexed as

AcetylcysteineAnimalsAnti-Inflammatory AgentsCell Cycle ProteinsCell LineCell ProliferationCell SurvivalGene Expression RegulationInterleukin-1betaLipopolysaccharidesMesenchymal Stem CellsNLR Family, Pyrin Domain-Containing 3 ProteinRatsSignal TransductionAcetylcysteineAnti-Inflammatory AgentsCell Cycle ProteinsIL1B protein, ratInterleukin-1betaLipopolysaccharidesNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, ratTXNIP protein, rat

Identifiers

PMID32945495
PMCPMC7453581
OpenAlexW3048928578

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.