Evidence map›Paper›PMID 31545489›Full record

ArticleMolecular medicine reports2019

Mechanism of glycyrrhizin on ferroptosis during acute liver failure by inhibiting oxidative stress.

Yao Wang, Qian Chen, Chunxia Shi, Fangzhou Jiao, Zuojiong Gong

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed, 1 pooled it
9.0field-weighted citation impact, top 1% 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

75 citing papers in PubMed, 1 synthesis or guideline pooled it, 122 citations in OpenAlex.

  1. Pooled it
  2. Review
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  5. Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Review
  12. Involvement of HMGB1-mediated ferroptosis in systemic diseases.Frontiers in cell and developmental biology · 2025
    Review
  13. Article
  14. Emerging Roles of High-mobility Group Box-1 in Liver Disease.Journal of clinical and translational hepatology · 2024
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Review

15 more citing papers are in PubMed but not listed here.

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

5 authors at 2 institutions in 1 country.

Yao WangDepartment of Infectious Diseases, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China.
Qian ChenDepartment of Infectious Diseases, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China.
Chunxia ShiDepartment of Infectious Diseases, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China.
Fangzhou JiaoDepartment of Infectious Diseases, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China.
Zuojiong GongDepartment of Infectious Diseases, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China.
Renmin Hospital of Wuhan University · CNWuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The present study aimed to investigate the anti‑ferroptosis effects of the HMGB1 inhibitor glycyrrhizin (GLY). The present study used a cell and animal model of acute liver failure (ALF), induced using tumor necrosis factor‑α, lipopolysaccharide and D‑galactosamine, to investigate the effects of GLY. The expression of glutathione peroxidase 4 (GPX4) and high mobility group protein B1 (HMGB1), heme oxygenase‑1 (HO‑1) and nuclear factor erythroid 2‑related factor 2 (Nrf2) were detected were detected by western blotting in L02 hepatocytes and mouse liver. The expression of GPX4 and HMGB1 in L02 hepatocytes and mouse liver was detected by immunofluorescence. The pathological changes to liver tissues were determined by hematoxylin and eosin staining. The levels of lactate dehydrogenase (LDH), Fe2+, reactive oxygen species (ROS) and glutathione (GSH) were tested using kits. Compared with the normal group, the degree of liver damage and liver function in the model animal group was severe. The protein levels of HMGB1 in L02 cells and liver tissues were significantly increased. The expression of NRF2, HO‑1 and GPX4 was significantly decreased. The levels of LDH, Fe2+, malondialdehyde (MDA) and ROS were increased, whereas the level of GSH was decreased. Treatment with GLY reduced the degree of liver damage, the expression of HMGB1 was decreased, and the levels of Nrf2, HO‑1 and GPX4 were increased. The levels of LDH, Fe2+, MDA, ROS were decreased, while the level of GSH was increased by GLY treatment. The results of the present study indicated that HMGB1 is involved in the process of ferroptosis. The HMGB1 inhibitor GLY significantly reduced the degree of ferroptosis during ALF by inhibiting oxidative stress.

Indexed as

AnimalsBiomarkersCells, CulturedCell SurvivalDisease Models, AnimalFerroptosisGlycyrrhizic AcidHeme Oxygenase-1HMGB1 ProteinHumansLiver Failure, AcuteMaleMiceOxidative StressReactive Oxygen SpeciesTumor Necrosis Factor-alphaBiomarkersGlycyrrhizic AcidHeme Oxygenase-1HMGB1 ProteinReactive Oxygen SpeciesTumor Necrosis Factor-alpha

Identifiers

PMID31545489
PMCPMC6797988
OpenAlexW2972923507

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.