Evidence map›Paper›PMID 31428632›Full record

ArticleBioMed research international2019

Protective Effect of Astragaloside IV on Hepatic Injury Induced by Iron Overload.

Dongyu Xie, Ping Zhou, Lin Liu, Wenjing Jiang, Haina Xie, Liang Zhang, Donghao Xie

Open access · hybridAbstract read
In one paragraph

Article in BioMed research international, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

16 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
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  7. Metal ions overloading and cell death.Cell biology and toxicology · 2024
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  12. Roots ofEvidence-based complementary and alternative medicine : eCAM · 2022
    Article
  13. Article
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  16. Chemical Discrimination ofMolecules (Basel, Switzerland) · 2019
    Article
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 5 institutions in 1 country.

Dongyu XieDepartment of Spleen-Stomach, Zhenjiang Affiliated Hospital of Nanjing University of Traditional Chinese Medicine, Zhenjiang, China.
Ping ZhouDepartment of Pharmacy, People's Hospital of Yangzhong City, Zhenjiang, China.
Lin LiuDepartment of Pharmacy, Dahua Hospital, Xuhui District, Shanghai, China.
Wenjing JiangDepartment of Pharmacy, Dahua Hospital, Xuhui District, Shanghai, China.
Haina XieSchool of Basic Medical Science, Shanghai University of Traditional Chinese Medicine, China.
Liang ZhangCollege of Pharmacy, Nanjing University of Chinese Medicine, China.ORCID https://orcid.org/0000-0002-4178-1101
Donghao XieDepartment of Pharmacy, Guanghua Hospital of Integrated Traditional Chinese and Western Medicine, Shanghai, China.ORCID https://orcid.org/0000-0003-2297-1628
Dahua Hospital · CNJiangsu University · CNNanjing University of Chinese Medicine · CNPeople's Hospital of Yangzhong · CNShanghai University of Traditional Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Suitable content of iron is essential for human body, but iron overload is associated with many kinds of diseases including chronic liver damage. Recently, researchers find that iron overload promotes hepatocyte autophagy and apoptosis. However, the mechanism of iron overload in liver damage remains unclear. In this study, Lo2 cells were selected as the research object, iron dextran was a model drug, and astragaloside IV was a therapeutic drug to explore the role of iron overload. MTT assay and Annexin/PI double staining were used to measure cell viability and apoptosis. Ultrastructure was observed by transmission electron microscopy. The expression levels of apoptosis and autophagy-related proteins were determined by real-time PCR and Western Blot. The results showed that iron dextran could significantly inhibit Lo2 cell viability and increase the apoptosis rate, while astragaloside IV could reverse the inhibition of Lo2 cell viability and decrease the apoptosis rate. Transmission electron microscopy showed a significant increase in the number of autophagosomes after administration of iron dextran, and the application of astragaloside IV reduced the production of autophagosomes. LC3II/I was significantly upregulated in the model group but decreased in the astragaloside IV treatment group, and P62 showed the opposite trend. Iron dextran significantly upregulated the expression of Bax and downregulated Bcl2, while astragaloside IV reversed this trend. Finally, the inhibition of hepcidin caused by iron dextran was counteracted by astragaloside IV. In conclusion, the experimental results show that the iron overload model mainly induces excessive autophagy and apoptosis of hepatocytes, thus causing damage to hepatocytes, but astragaloside IV plays a certain therapeutic role in reversing this damage.

Indexed as

Autophagosomesbcl-2-Associated X ProteinCell LineCell SurvivalHepatocytesHumansIron-Dextran ComplexIron OverloadLiverMicrotubule-Associated ProteinsProto-Oncogene Proteins c-bcl-2RNA-Binding ProteinsSaponinsTriterpenesastragaloside ABAX protein, humanbcl-2-Associated X ProteinBCL2 protein, humanIron-Dextran ComplexMAP1LC3A protein, humanMAP1LC3B protein, humanMicrotubule-Associated ProteinsP62 protein, humanProto-Oncogene Proteins c-bcl-2RNA-Binding ProteinsSaponinsTriterpenes

Identifiers

PMID31428632
PMCPMC6683835
OpenAlexW2963589894

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.