Evidence map›Paper›PMID 32410985›Full record

ArticleFrontiers in pharmacology2020

Proteomics Unravels Emodin Causes Liver Oxidative Damage Elicited by Mitochondrial Dysfunction.

Yinhuan Zhang, Xiaowei Yang, Zhixin Jia, Jie Liu, Xiaoning Yan, Yihang Dai, Hongbin Xiao

Open access · goldAbstract read
In one paragraph

Article in Frontiers in pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.6field-weighted citation impact, top 15% 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

13 citing papers in PubMed, 18 citations in OpenAlex.

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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 2 institutions in 1 country.

Yinhuan ZhangResearch Center of Chinese Medicine Analysis and Transformation, Beijing University of Chinese Medicine, Beijing, China.
Xiaowei YangInstitute of Chinese Materia Medica, China Academy of Chinese Medical Sciences, Beijing, China.
Zhixin JiaResearch Center of Chinese Medicine Analysis and Transformation, Beijing University of Chinese Medicine, Beijing, China.
Jie LiuResearch Center of Chinese Medicine Analysis and Transformation, Beijing University of Chinese Medicine, Beijing, China.
Xiaoning YanResearch Center of Chinese Medicine Analysis and Transformation, Beijing University of Chinese Medicine, Beijing, China.
Yihang DaiResearch Center of Chinese Medicine Analysis and Transformation, Beijing University of Chinese Medicine, Beijing, China.
Hongbin XiaoResearch Center of Chinese Medicine Analysis and Transformation, Beijing University of Chinese Medicine, Beijing, China.
Beijing University of Chinese Medicine · CNChinese Academy of Medical Sciences & Peking Union Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Emodin is one of the main active compounds in many Chinese traditional herbs. Due to its potential toxic effect on the liver, the possible injury mechanism needs to be explored. In the present study, we investigated liver injury mechanisms of emodin on rats by the technology of proteomics. Firstly, 4530 proteins were identified from the liver of rats treated with emodin by label free proteomics. Inside, 892 differential proteins were selected, presenting a downward trend. Bioinformatics analysis showed that proteins interfered with by emodin were mainly involved in oxidation-reduction biological processes and mitochondrial metabolic pathways, such as mitochondrial fatty acid β-oxidation, citric acid cycle, and oxidative phosphorylation, which were further confirmed by western blot. The decrease in maximal respiration, ATP production, spare respiratory capacity, and coupling efficiency and increase in proton leakage were detected by seahorse XFe 24 analyzer, which confirmed the damage of mitochondrial function. The down-regulated expressions in antioxidant proteins were verified by western blot and a significant increase of ROS levels were detected in emodin group, which showed that emodin disrupted redox homeostasis in livers. Molecular docking revealed that the main targets of emodin might be acadvl and complex IV. Generally, emodin could induce oxidative stress in livers by directly targeting acadvl/complex IV and inhibiting fatty acid β-oxidation, citric acid cycle, and oxidative phosphorylation taken place in mitochondria.

Indexed as

Emodinliver injurymitochondrial dysfunctionproteomicsredox homeostasis

Identifiers

PMID32410985
PMCPMC7201015
OpenAlexW3021002616

What OpenQuestion holds

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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.