Evidence map›Paper›PMID 31694300›Full record

ArticleBiomolecules2019

Curcumin Ameliorates Lead-Induced Hepatotoxicity by Suppressing Oxidative Stress and Inflammation, and Modulating Akt/GSK-3β Signaling Pathway.

Ahlam Alhusaini, Laila Fadda, Iman H Hasan, Enas Zakaria, Abeer M Alenazi, Ayman M Mahmoud

Open access · goldAbstract read
In one paragraph

Article in Biomolecules, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

31 citing papers in PubMed, 63 citations in OpenAlex.

  1. Potential Antidote Against Lead Toxicity-A Review.International journal of molecular sciences · 2026
    Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
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  12. A Review of the Role of Curcumin in Metal Induced Toxicity.Antioxidants (Basel, Switzerland) · 2023
    Review
  13. Article
  14. Article
  15. Antioxidants (Basel, Switzerland) · 2022
    Article
  16. Article
  17. Article
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  19. Review
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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

6 authors at 2 institutions in 2 countries.

Ahlam AlhusainiPharmacology and Toxicology Department, Faculty of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia.
Laila FaddaPharmacology and Toxicology Department, Faculty of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia.
Iman H HasanPharmacology and Toxicology Department, Faculty of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia.
Enas ZakariaPharmaceutics Department, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia.
Abeer M AlenaziPharmacology and Toxicology Department, Faculty of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia.
Ayman M MahmoudPhysiology Division, Zoology Department, Faculty of Science, Beni-Suef University, Beni-Suef 62514, Egypt.ORCID 0000-0003-0279-6500
King Saud University · SABeni-Suef University · EG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lead (Pb) is a toxic heavy metal pollutant with adverse effects on the liver and other body organs. Curcumin (CUR) is the principal curcuminoid of turmeric and possesses strong antioxidant and anti-inflammatory activities. This study explored the protective effect of CUR on Pb hepatotoxicity with an emphasis on oxidative stress, inflammation and Akt/GSK-3β signaling. Rats received lead acetate and CUR and/or ascorbic acid (AA) for seven days and samples were collected for analyses. Pb(II) induced liver injury manifested by elevated serum alanine aminotransferase (ALT), aspartate aminotransferase (AST) and lactate dehydrogenase (LDH), as well as histopathological alterations, including massive hepatocyte degeneration and increased collagen deposition. Lipid peroxidation, nitric oxide, TNF-α and DNA fragmentation were increased, whereas antioxidant defenses were diminished in the liver of Pb(II)-intoxicated rats. Pb(II) increased hepatic NF-κB and JNK phosphorylation and caspase-3 cleavage, whereas Akt and GSK-3β phosphorylation was decreased. CUR and/or AA ameliorated liver function, prevented tissue injury, and suppressed oxidative stress, DNA damage, NF-κB, JNK and caspase-3. In addition, CUR and/or AA activated Akt and inhibited GSK-3β in Pb(II)-induced rats. In conclusion, CUR prevents Pb(II) hepatotoxicity via attenuation of oxidative injury and inflammation, activation of Akt and inhibition of GSK-3β. However, further studies scrutinizing the exact role of Akt/GSK-3β signaling are recommended.

Indexed as

Alanine TransaminaseAnimalsAnti-Inflammatory AgentsAscorbic AcidAspartate AminotransferasesChemical and Drug Induced Liver InjuryCurcuminDisease Models, AnimalGene Expression Regulation, EnzymologicGlycogen Synthase Kinase 3 betaL-Lactate DehydrogenaseMaleOrganometallic CompoundsOxidative StressPhosphorylationProto-Oncogene Proteins c-aktAlanine TransaminaseAnti-Inflammatory AgentsAscorbic AcidAspartate AminotransferasesCurcuminGlycogen Synthase Kinase 3 betalead acetateL-Lactate DehydrogenaseOrganometallic CompoundsProto-Oncogene Proteins c-aktCurcuminGSK-3βJNKLeadNF-κBoxidative stress

Identifiers

PMID31694300
PMCPMC6920970
OpenAlexW2988215093

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.