Evidence map›Paper›PMID 30952839›Full record

ArticleCell death & disease2019

Nrf2 signaling and autophagy are complementary in protecting lipopolysaccharide/d-galactosamine-induced acute liver injury by licochalcone A.

Hongming Lv, Huahong Yang, Zhongfeng Wang, Haihua Feng, Xuming Deng, Genhong Cheng, Xinxin Ci

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
15.1field-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

53 citing papers in PubMed, 117 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Autophagy in the liver.Autophagy reports · 2026
    Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Review
  19. Article
  20. Article
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

7 authors at 3 institutions in 2 countries.

Hongming LvInstitute of Translational Medicine, The First Hospital, Jilin University, 130001, Changchun, China.
Huahong YangInstitute of Translational Medicine, The First Hospital, Jilin University, 130001, Changchun, China.
Zhongfeng WangInstitute of Translational Medicine, The First Hospital, Jilin University, 130001, Changchun, China.
Haihua FengKey Laboratory of Zoonosis, Ministry of Education, Institute of Zoonosis, College of Veterinary Medicine, Jilin University, Changchun, China.
Xuming DengKey Laboratory of Zoonosis, Ministry of Education, Institute of Zoonosis, College of Veterinary Medicine, Jilin University, Changchun, China.
Genhong ChengInstitute of Translational Medicine, The First Hospital, Jilin University, 130001, Changchun, China.
Xinxin CiInstitute of Translational Medicine, The First Hospital, Jilin University, 130001, Changchun, China. cixinxin@jlu.edu.cn.
Jilin University · CNFirst Hospital of Jilin University · CNUniversity of California, Los Angeles · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Licochalcone A (Lico A), isolated from Xinjiang licorice Glycyrrhiza inflate, has been shown to have antioxidative potential via the activation of nuclear factor-erythroid 2-related factor 2 (Nrf2) activation, which is involved in the prevention of acetaminophen-induced hepatotoxicity. The purpose of the current study was to further explore the protective effect of Lico A against lipopolysaccharide/d-galactosamine (LPS/GalN)-induced acute liver injury (ALI) and its underlying molecular mechanisms. Our results found that treatment with Lico A significantly reduced in LPS/GalN-induced hepatotoxicity by lessening lethality, alleviating histopathological liver changes, decreasing the alanine transaminase, and aspartate aminotransferase levels, attenuating the secretion of inflammatory cytokines, and regulating oxidative markers. Furthermore, Lico A efficiently alleviated LPS-induced inflammatory response by inhibiting TLR4-MAPK and -NF-κB, as well as the Txnip-NLRP3 signaling pathway. Meanwhile, Lico A induced the activation of Nrf2 and QSTM1 (P62) signaling and promoted autophagy involved in AMP-activated protein kinase (AMPK)-the transcription factor EB (TFEB) signaling, which may contribute to its hepatoprotective activity. Additional mechanistic investigations to evaluate the dependence of the hepatoprotective role of Lico A on Nrf2 revealed that a lack of Nrf2 promoted Lico A-induced autophagy, which contributed to the hepatoprotective effect of Lico A in Nrf2

Indexed as

AnimalsAutophagyCarrier ProteinsChalconesChemical and Drug Induced Liver InjuryCytokinesGalactosamineInflammasomesLipopolysaccharidesMaleMAP Kinase Signaling SystemMiceMice, Inbred C57BLMice, KnockoutNF-E2-Related Factor 2NF-kappa BCarrier ProteinsChalconesCytokinesGalactosamineGtf2h1 protein, mouseInflammasomeslicochalcone ALipopolysaccharidesNFE2L2 protein, humanNF-E2-Related Factor 2NF-kappa BProtective AgentsReactive Oxygen SpeciesThioredoxinsTranscription Factor TFIIHTxnip protein, mouse

Identifiers

PMID30952839
PMCPMC6450927
OpenAlexW2927221756

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.