Evidence map›Paper›PMID 30944389›Full record

ArticleScientific reports2019

Glucosamine inhibits IL-1β expression by preserving mitochondrial integrity and disrupting assembly of the NLRP3 inflammasome.

Hsiao-Wen Chiu, Lan-Hui Li, Chih-Yu Hsieh, Yerra Koteswara Rao, Fang-Hsin Chen, Ann Chen, Shuk-Man Ka, Kuo-Feng Hua

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
3.1field-weighted citation impact, top 8% 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

30 citing papers in PubMed, 1 synthesis or guideline pooled it, 64 citations in OpenAlex.

  1. Pooled it
  2. Glucosamine as a regulator of O-GlcNAc signaling: linking metabolism to disease pathogenesis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review
  3. Article
  4. Article
  5. Neuroprotective Effects of Glucosamine in Huntington's Disease Through NLRP3 Inflammasome Inhibition.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025
    Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Role of mitochondrial stress and the NLRP3 inflammasome in lung diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023
    Review
  14. Article
  15. Review
  16. Article
  17. Article
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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

8 authors at 5 institutions in 1 country.

Hsiao-Wen ChiuGraduate Institute of Life Science, National Defense Medical Center, Taipei, Taiwan.
Lan-Hui LiDepartment of Laboratory Medicine, Linsen, Chinese Medicine and Kunming Branch, Taipei City Hospital, Taipei, Taiwan.
Chih-Yu HsiehDepartment of Biotechnology and Animal Science, National Ilan University, Ilan, Taiwan.ORCID http://orcid.org/0000-0001-9770-6779
Yerra Koteswara RaoDepartment of Biotechnology and Animal Science, National Ilan University, Ilan, Taiwan.
Fang-Hsin ChenDepartment of Medical Imaging and Radiological Sciences, Chang Gung University, Taoyuan, Taiwan.ORCID http://orcid.org/0000-0002-1671-4863
Ann ChenDepartments of Pathology, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan.
Shuk-Man KaGraduate Institute of Life Science, National Defense Medical Center, Taipei, Taiwan. shukmanka@gmail.com.
Kuo-Feng HuaDepartment of Biotechnology and Animal Science, National Ilan University, Ilan, Taiwan. kuofenghua@gmail.com.ORCID http://orcid.org/0000-0001-8436-8299
National Defense Medical Center · TWNational Ilan University · TWTri-Service General Hospital · TWChang Gung University · TWTaipei City Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The NLRP3 inflammasome promotes the pathogenesis of metabolic, neurodegenerative and infectious diseases. Increasing evidences show that the NLRP3 inflammasome is a promising therapeutic target in inflammatory diseases. Glucosamine is widely used as a dietary supplement to promote the health of cartilage tissue and is expected to exert anti-inflammatory activity in joint inflammation, which is a nucleotide-binding oligomerization domain-like receptor containing pyrin domain 3 (NLRP3) inflammasome-associated complication. Here, we investigated whether GlcN inhibits the NLRP3 inflammasome and dissected the underlying molecular mechanisms. We found that GlcN suppressed the NLRP3 inflammasome in mouse and human macrophages. A mechanistic study revealed that GlcN inhibited the expression of NLRP3 and IL-1β precursor by reducing reactive oxygen species generation and NF-κB activation in lipopolysaccharide-activated macrophages. GlcN also suppressed mitochondrial reactive oxygen species generation and mitochondrial integrity loss in NLRP3-activated macrophages. Additionally, GlcN disrupted NLRP3 inflammasome assembly by inhibiting NLRP3 binding to PKR, NEK7 and ASC. Furthermore, oral administration of GlcN reduced peritoneal neutrophils influx and lavage fluids concentrations of IL-1β, IL-6 MCP-1 and TNF-α in uric acid crystal-injected mice. These results indicated that GlcN might be a novel dietary supplement for the amelioration of NLRP3 inflammasome-associated complications.

Indexed as

AnimalsCell LineGlucosamineHumansInflammasomesInflammationInterleukin-1betaMacrophagesMaleMiceMice, Inbred C57BLMitochondriaNLR Family, Pyrin Domain-Containing 3 ProteinReactive Oxygen SpeciesSignal TransductionTHP-1 CellsGlucosamineIL1B protein, humanInflammasomesInterleukin-1betaNLR Family, Pyrin Domain-Containing 3 ProteinNLRP3 protein, humanReactive Oxygen Species

Identifiers

PMID30944389
PMCPMC6447579
OpenAlexW2926746486

What OpenQuestion holds

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LicenceCC BY
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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.