Evidence map›Paper›PMID 28498799›Full record

ArticleOncotarget2017

Dietary luteolin attenuates chronic liver injury induced by mercuric chloride via the Nrf2/NF-κB/P53 signaling pathway in rats.

Haili Zhang, Xiao Tan, Daqian Yang, Jingjing Lu, Biying Liu, Ruiqi Baiyun, Zhigang Zhang

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
7.1field-weighted citation impact, top 3% 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

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 65 citations in OpenAlex.

  1. Pooled it
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  15. The Role of Toxic Metals and Metalloids in Nrf2 Signaling.Antioxidants (Basel, Switzerland) · 2021
    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

7 authors at 1 institution in 1 country.

Haili ZhangCollege of Veterinary Medicine, Northeast Agricultural University, Harbin, 150030, China.
Xiao TanCollege of Veterinary Medicine, Northeast Agricultural University, Harbin, 150030, China.
Daqian YangCollege of Veterinary Medicine, Northeast Agricultural University, Harbin, 150030, China.
Jingjing LuCollege of Veterinary Medicine, Northeast Agricultural University, Harbin, 150030, China.
Biying LiuCollege of Veterinary Medicine, Northeast Agricultural University, Harbin, 150030, China.
Ruiqi BaiyunCollege of Veterinary Medicine, Northeast Agricultural University, Harbin, 150030, China.
Zhigang ZhangCollege of Veterinary Medicine, Northeast Agricultural University, Harbin, 150030, China.
Northeast Agricultural University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mercury exposure is a common cause of metal poisoning which is biotransformed to highly toxic metabolites thus eliciting biochemical alterations and oxidative stress. Luteolin, a phenolic compound found in many natural products, has multiple biological functions. Our study was aimed to explore the biological effects of luteolin in a liver injury model induced in rats by mercuric chloride (HgCl2). Criteria for injury included liver enzyme, glutathione and malondialdehyde levels, histopathology, TUNEL assay, hepatocyte viability and reactive oxygen species levels. The results showed that luteolin protected against HgCl2-induced liver injury. Luteolin increased total nuclear factor-erythroid-2-related factor 2 (Nrf2) levels in the presence of HgCl2. Upregulation of its downstream factors, heme oxygenase-1 and NAD(P)H quinone oxidoreductase 1, was also observed. This suggested that protection by luteolin against HgCl2-induced liver injury involved Nrf2 pathway activation. Luteolin also decreased expression of nuclear factor-κB (NF-κB) and P53. HgCl2 exposure led to increased Bcl-associated X protein (Bax), and decreased Bcl-2-related protein long form of Bcl-x (Bcl-xL) and B-cell leukemia/lymphoma-2 (Bcl-2) expression, leading to an increased Bax/Bcl-2 ratio. Taken together, our data suggested that decreasing oxidative stress is a protective mechanism of luteolin against development of HgCl2-induced liver injury, through the Nrf2/NF-κB/P53 signaling pathway in rats.

Indexed as

AnimalsChemical and Drug Induced Liver InjuryChronic DiseaseDietary SupplementsHeme Oxygenase-1HepatocytesLiverLuteolinMercuric ChlorideNAD(P)H Dehydrogenase (Quinone)NF-E2-Related Factor 2NF-kappa BOxidative StressProtective AgentsRats, WistarSignal TransductionHeme Oxygenase-1LuteolinMercuric ChlorideNAD(P)H Dehydrogenase (Quinone)Nfe2l2 protein, ratNF-E2-Related Factor 2NF-kappa BProtective AgentsTumor Suppressor Protein p53hepatotoxicityHgCl2luteolinNF-κBNrf2

Identifiers

PMID28498799
PMCPMC5522226
OpenAlexW2605851091

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.