Evidence map›Paper›PMID 30150561›Full record

ArticleMarine drugs2018

Protective Effect of Eckol against Acute Hepatic Injury Induced by Carbon Tetrachloride in Mice.

Shulan Li, Juan Liu, Mengya Zhang, Yuan Chen, Tianxing Zhu, Jun Wang

Abstract read
In one paragraph

Article in Marine drugs, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

15 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Alkaloids in Tibetan MedicineMolecules (Basel, Switzerland) · 2025
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  5. Review
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  8. Hepatoprotective Polysaccharides fromMolecules (Basel, Switzerland) · 2022
    Article
  9. Silibinin Schiff Base Derivatives Counteract CClDrug design, development and therapy · 2022
    Article
  10. Review
  11. Review
  12. Article
  13. Review
  14. Eckol fromNutrients · 2020
    Article
  15. 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

6 authors.

Shulan LiDepartment of Pharmacology, College of Medicine, Wuhan University of Science and Technology, Wuhan 430065, China. lishulan971204@outlook.com.
Juan LiuDepartment of Pharmacology, College of Medicine, Wuhan University of Science and Technology, Wuhan 430065, China. liujuan79@wust.edu.cn.
Mengya ZhangDepartment of Pharmacology, College of Medicine, Wuhan University of Science and Technology, Wuhan 430065, China. zhangmengya0703@163.com.
Yuan ChenDepartment of Pharmacology, College of Medicine, Wuhan University of Science and Technology, Wuhan 430065, China. susiechen1997@163.com.
Tianxing ZhuDepartment of Pharmacology, College of Medicine, Wuhan University of Science and Technology, Wuhan 430065, China. Yaoxue.xi@163.com.
Jun WangDepartment of Pharmacology, College of Medicine, Wuhan University of Science and Technology, Wuhan 430065, China. wangjun@wust.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Several in vitro studies have shown the potential hepatoprotective properties of eckol, a natural phlorotannin derived from the brown alga. However, the in vivo hepatoprotective potential of eckol has not been determined. In this study, we performed an in vivo study to investigate the protective effect of eckol and its possible mechanisms on the carbon tetrachloride (CCl₄)-induced acute liver injury model in mice. Results revealed that eckol pre-treatment at the dose of 0.5 and 1.0 mg/kg/day for 7 days significantly suppressed the CCl₄-induced increases of alanine transaminase (ALT) and aspartate aminotransferase (AST) levels in serum and meliorated morphological liver injury. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling (TUNEL) analysis showed that the number of positive apoptotic hepatocytes in the eckol-treated group was lower than that in the CCl₄ model group. Western blotting analysis also demonstrated the enhanced expression of bcl-2 and suppressed expression of cleaved caspase-3 by eckol. The CCl₄-induced oxidative stress in liver was significantly ameliorated by eckol, which was characterized by reduced malondialdehyde (MDA) formations, and enhanced superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) activities and glutathione (GSH) content. Moreover, the CCl₄-induced elevations of pro-inflammatory cytokines tumor necrosis factor (TNF)-α, interleukin (IL)-1β and IL-6 were markedly suppressed in the eckol-treated group. However, eckol enhanced the level of IL-10, a potent anti-inflammatory cytokine, and recruited CD11c⁺ dendritic cells into the liver tissues of CCl₄-treated mice. These results indicated that eckol has the protective effect on CCl₄-induced acute liver injury via multiple mechanisms including anti-apoptosis, anti-oxidation, anti-inflammation and immune regulation.

Indexed as

AnimalsApoptosisBiological ProductsCarbon TetrachlorideChemical and Drug Induced Liver InjuryCytokinesDendritic CellsDioxinsDisease Models, AnimalHumansLiverMaleMiceOxidative StressPhaeophyceaeProtective AgentsBiological ProductsCarbon TetrachlorideCytokinesDioxinseckolProtective Agentsacute liver injuryapoptosisdendritic cellseckolinflammationoxidative stress

Identifiers

PMID30150561
PMCPMC6164428

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Registered trials

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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.