Evidence map›Paper›PMID 24531650›Full record

ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2014

Oxidative stress promotes D-GalN/LPS-induced acute hepatotoxicity by increasing glycogen synthase kinase 3β activity.

Linlin Wei, Feng Ren, Xiangying Zhang, Tao Wen, Hongbo Shi, Sujun Zheng, Jing Zhang, Yu Chen, Yuanping Han, Zhongping Duan

Open access · hybridAbstract read
In one paragraph

Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
5.3field-weighted citation impact, top 5% 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

29 citing papers in PubMed, 44 citations in OpenAlex.

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  12. Nutrients · 2020
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  17. Pretreatment WithFrontiers in microbiology · 2019
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  18. A Phenolic Acid and Flavonoid Fraction Isolated fromIndian journal of clinical biochemistry : IJCB · 2019
    Article
  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

10 authors at 3 institutions in 1 country.

Linlin WeiBeijing Artificial Liver Treatments & Training Center, Beijing YouAn Hospital, Capital Medical University, Beijing, China.
Feng Ren
Xiangying Zhang
Tao Wen
Hongbo Shi
Sujun Zheng
Jing Zhang
Yu Chen
Yuanping Han
Zhongping Duan
Beijing YouAn Hospital · CNCapital Medical University · CNSichuan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveOur previous studies have demonstrated that glycogen synthase kinase 3β (GSK3β) activity is increased in the progression of acute liver failure (ALF), which aggravates liver injury, while its regulatory mechanism remains elusive. This study is designated to address whether oxidative stress activates GSK3β to promote ALF.

methodsIn a murine model induced by D-galactosamine (D-GalN) (700 mg/kg) and LPS (10 μg/kg), N-acetylcysteine (300 mg/kg) or SB216763 (25 mg/kg) was used to inhibit oxidative stress or GSK3β activity, respectively. Serum alanine aminotransferase and aspartate aminotransferase levels were assessed. The parameters of oxidative stress were evaluated in liver tissue. Whether GSK3β inhibition protects hepatocytes from oxidative stress-induced cell apoptosis was investigated in vitro. Moreover, the activity of GSK3β was measured in the liver of chronic hepatitis B (CHB) patients and ALF patients.

resultsIn vivo, N-acetylcysteine ameliorated the D-GalN/LPS-induced hepatotoxicity and reduced GSK3β activity; GSK3β inhibition increased hepatic superoxide dismutase activity and the glutathione content, decreased malondialdehyde production in the liver tissues; while GSK3β inhibition suppressed the JNK activation in the liver and decreased cytochrome c release from mitochondria. In vitro, GSK3β inhibition lessened hepatocytes apoptosis induced by H2O2 or Antimycin A, as demonstrated by decreased LDH activity, and reduced cleavage of caspase-3 expression. Furthermore, GSK3β activity in the CHB patients was increased in the phase of ALF.

conclusionsResults indicate that GSK3β activation contributes to liver injury by participating in oxidative stress response in ALF and is, therefore, a potential therapeutic target for ALF.

Indexed as

AdultAlanine TransaminaseAnimalsAspartate AminotransferasesCell LineFemaleGalactosamineGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHepatitis B, ChronicHumansLipopolysaccharidesLiver Failure, AcuteMaleMice, Inbred C57BLMiddle AgedAlanine TransaminaseAspartate AminotransferasesGalactosamineGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGSK3B protein, humanGsk3b protein, mouseLipopolysaccharides

Identifiers

PMID24531650
PMCPMC4018480
OpenAlexW2010475904

What OpenQuestion holds

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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.