Evidence map›Paper›PMID 37397929›Full record

ArticleToxicology research2023

Hepatoprotective effect of avicularin on lead-induced steatosis, oxidative stress, and inflammation in mice associated with the MAPK/HSP60/NLRP3 and SREBP1c pathway.

Ting Qiu, Jia-Xue Shi, Chao Cheng, Hong Jiang, Hai-Nan Ruan, Jun Li, Chan-Min Liu

Open access · greenAbstract read
In one paragraph

Article in Toxicology research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.6field-weighted citation impact, top 20% 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

9 citing papers in PubMed, 10 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Chaperonin in health and disease.Molecular biomedicine · 2026
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Molecular Chaperonin HSP60: Current Understanding and Future Prospects.International journal of molecular sciences · 2024
    Review
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.

Ting QiuSchool of Life Science, Jiangsu Normal University, No.101, Shanghai Road, Tongshan New Area, Xuzhou City, Jiangsu Province 21-1116, PR China.
Jia-Xue ShiSchool of Life Science, Jiangsu Normal University, No.101, Shanghai Road, Tongshan New Area, Xuzhou City, Jiangsu Province 21-1116, PR China.
Chao ChengSchool of Life Science, Jiangsu Normal University, No.101, Shanghai Road, Tongshan New Area, Xuzhou City, Jiangsu Province 21-1116, PR China.
Hong JiangSchool of Life Science, Jiangsu Normal University, No.101, Shanghai Road, Tongshan New Area, Xuzhou City, Jiangsu Province 21-1116, PR China.
Hai-Nan RuanSchool of Life Science, Jiangsu Normal University, No.101, Shanghai Road, Tongshan New Area, Xuzhou City, Jiangsu Province 21-1116, PR China.
Jun LiSchool of Life Science, Jiangsu Normal University, No.101, Shanghai Road, Tongshan New Area, Xuzhou City, Jiangsu Province 21-1116, PR China.
Chan-Min LiuSchool of Life Science, Jiangsu Normal University, No.101, Shanghai Road, Tongshan New Area, Xuzhou City, Jiangsu Province 21-1116, PR China.
Jiangsu Normal University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lead (Pb), an environmental hazard, causes severe diseases in the liver, kidney, cardiovascular system, hematopoietic system, reproductive system, and nervous system. Avicularin (AVI), the main dietary flavonoid found in many citrus fruits, exhibited potential protective properties on organs. However, the molecular mechanisms of these protective actions are currently not clear. In our study, the effects of AVI on Pb-induced hepatotoxicity were evaluated using ICR mice. Changes in oxidative stress, inflammation, lipid metabolism, and related signaling were evaluated. We found for the first time that treatment with AVI significantly reduced hepatic steatosis, inflammation, and oxidative stress induced by Pb. AVI attenuated Pb-induced liver dysfunction and lipid metabolism disorder in mice. AVI decreased the serum biochemical indicators of lipid metabolism. AVI decreased the expression levels of lipid metabolism-related protein SREBP-1c, acetyl-CoA carboxylase (ACC), and FAS. AVI suppressed Pb-induced inflammation in livers, as indicated by decreasing the TNF-α and IL-1β levels. AVI suppressed oxidative stress by increasing the activation of SOD, CAT, and GPx. Furthermore, AVI inhibited the activities of JNK, ERK, p38, and NF-κB. AVI further decreased the levels of HSP60, NLRP3, p-IκBα, and p-p65 in the livers of mice. Collectively, this study indicated that AVI mitigated Pb-induced hepatic steatosis, oxidative stress, and inflammation by regulating the SREBP-1c and MAPK/HSP60/NLRP3 signaling pathways.

Indexed as

aviponcirinhepatic steatosisinflammationleadoxidative stressSREBP1c

Identifiers

PMID37397929
PMCPMC10311149
OpenAlexW4366758571

What Socratic holds

Textmetadata
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 Socratic graph.