Evidence map›Paper›PMID 38755566›Full record

ArticleBMC complementary medicine and therapies2024

Luteolin attenuates CCl4-induced hepatic injury by inhibiting ferroptosis via SLC7A11.

Zhiqiang Han, Batudeligen, Hongmei Chen, Narisu, Anda, Yanhua Xu, Lan Xue

Abstract read
In one paragraph

Article in BMC complementary medicine and therapies, 2024. 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
–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

16 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Targeted delivery of berberineNanoscale advances · 2026
    Article
  8. Review
  9. Article
  10. Review
  11. Artesunate induces ferroptosis in osteosarcoma through NCOA4-mediated ferritinophagy.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  12. Review
  13. Review
  14. Review
  15. Luteolin for the Treatment of Organ Fibrosis: A Mini Review.Mini reviews in medicinal chemistry · 2025
    Review
  16. 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.

Zhiqiang HanInstitute of Clinical Pharmacology of Traditional Mongolian Medicine, Affiliated Hospital of Inner Mongolia Minzu University, No.1742, Huolinhe Street, Horqin Area, Tongliao City, Autonomous Region of Inner Mongolia, 028000, China. hanzhiqiang80@163.com.
BatudeligenInstitute of Clinical Pharmacology of Traditional Mongolian Medicine, Affiliated Hospital of Inner Mongolia Minzu University, No.1742, Huolinhe Street, Horqin Area, Tongliao City, Autonomous Region of Inner Mongolia, 028000, China.
Hongmei ChenInstitute of Clinical Pharmacology of Traditional Mongolian Medicine, Affiliated Hospital of Inner Mongolia Minzu University, No.1742, Huolinhe Street, Horqin Area, Tongliao City, Autonomous Region of Inner Mongolia, 028000, China.
NarisuInstitute of Clinical Pharmacology of Traditional Mongolian Medicine, Affiliated Hospital of Inner Mongolia Minzu University, No.1742, Huolinhe Street, Horqin Area, Tongliao City, Autonomous Region of Inner Mongolia, 028000, China.
AndaInstitute of Clinical Pharmacology of Traditional Mongolian Medicine, Affiliated Hospital of Inner Mongolia Minzu University, No.1742, Huolinhe Street, Horqin Area, Tongliao City, Autonomous Region of Inner Mongolia, 028000, China.
Yanhua XuInstitute of Clinical Pharmacology of Traditional Mongolian Medicine, Affiliated Hospital of Inner Mongolia Minzu University, No.1742, Huolinhe Street, Horqin Area, Tongliao City, Autonomous Region of Inner Mongolia, 028000, China.
Lan XueInstitute of Clinical Pharmacology of Traditional Mongolian Medicine, Affiliated Hospital of Inner Mongolia Minzu University, No.1742, Huolinhe Street, Horqin Area, Tongliao City, Autonomous Region of Inner Mongolia, 028000, China.

Funding

National Natural Science Foundation of China 81860891the Young and Middle-aged Leading Talents Project Founding of Traditional Chinese Medicine (Mongolian Medicine) in Inner Mongolia Autonomous Region 2022 RC-005
6 · The paper itself

Abstract

backgroundLuteolin (3,4,5,7-tetrahydroxy flavone) is reported to strongly protect from acute carbon tetrachloride (CCl

methodsMice model and cell model of liver injury were constructed or induced to explore the effect and molecular mechanisms of Luteolin in the treatment of hepatic injury using CCl4. Cell Counting Kit-8 (CCK-8) and flow cytometry were used to evaluate HepG2 cell viability and apoptosis. The differential expressed genes involved in liver injury were scanned using RNA-seq and confirmed using functional study. Western blot was used to detect the indicators related to ferroptosis.

resultsLuteolin attenuated hepatic injury by alleviating cell morphology and decreasing serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphatase (ALP) levels in vivo mice models, and increasing cell viability, downregulating arachidonate 12-lipoxygenase (ALOX12), cyclooxygenase-2 (COX-2) and P21 protein expression, suppressing apoptosis in vitro cell models. Luteolin also inhibited ferroptosis by stimulating glutathione peroxidase 4 (GPX4) and mitochondrial ferritin (FTMT) protein expression, increasing glutathione (GSH) content, and minimizing Fe

conclusionLuteolin attenuated CCl

Indexed as

Amino Acid Transport System y+Carbon TetrachlorideChemical and Drug Induced Liver InjuryFerroptosisLuteolinAnimalsDisease Models, AnimalHep G2 CellsHumansMaleMiceMice, Inbred C57BLAmino Acid Transport System y+Carbon TetrachlorideLuteolinSLC7A11 protein, humanSlc7a11 protein, mouseFerroptosisGPX4Hepatic injuryLuteolinSLC7A11

Identifiers

PMID38755566
PMCPMC11100030

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.