Evidence map›Paper›PMID 27187341›Full record

ArticleMolecules (Basel, Switzerland)2016

The Mechanism by Which Amentoflavone Improves Insulin Resistance in HepG2 Cells.

Xiaoke Zheng, Yingying Ke, Aozi Feng, Peipei Yuan, Jing Zhou, Yang Yu, Xiaolan Wang, Weisheng Feng

Open access · goldAbstract read
In one paragraph

Article in Molecules (Basel, Switzerland), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

27 citing papers in PubMed, 53 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Establishment and Evaluation of HepG2 Cell Insulin Resistance Model.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025
    Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. AInternational journal of molecular sciences · 2022
    Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. The total flavonoids fromIranian journal of basic medical sciences · 2020
    Article
  18. Total flavonoids ofBiomedical reports · 2020
    Article
  19. Ethyl Acetate Extract ofFrontiers in pharmacology · 2020
    Article
  20. 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

8 authors at 1 institution in 1 country.

Xiaoke ZhengSchool of Pharmacy, Henan University of Traditional Chinese Medicine, Zhengzhou 450046, China. Zhengxk.2006@163.com.
Yingying KeSchool of Pharmacy, Henan University of Traditional Chinese Medicine, Zhengzhou 450046, China. keyingying1988@sina.com.
Aozi FengCenter for Artery Atheroscerosis Research, Havana University of Medical Sciences, Havana 999075, Cuba. fengaozi1987@sina.com.
Peipei YuanSchool of Pharmacy, Henan University of Traditional Chinese Medicine, Zhengzhou 450046, China. 15136153630@163.com.
Jing ZhouSchool of Pharmacy, Henan University of Traditional Chinese Medicine, Zhengzhou 450046, China. zhoujj1988326@sina.com.
Yang YuSchool of Pharmacy, Henan University of Traditional Chinese Medicine, Zhengzhou 450046, China. ku_rong@126.com.
Xiaolan WangSchool of Pharmacy, Henan University of Traditional Chinese Medicine, Zhengzhou 450046, China. wxl_325@163.com.
Weisheng FengSchool of Pharmacy, Henan University of Traditional Chinese Medicine, Zhengzhou 450046, China. fwsh@hactcm.edu.cn.
Henan University of Traditional Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe aim of this study was to explore the mechanism by which amentoflavone (AME) improves insulin resistance in a human hepatocellular liver carcinoma cell line (HepG2).

methodsA model of insulin resistant cells was established in HepG2 by treatment with high glucose and insulin. The glucose oxidase method was used to detect the glucose consumption in each group. To determine the mechanism by which AME improves insulin resistance in HepG2 cells, enzyme-linked immunosorbent assay (ELISA) and western blotting were used to detect the expression of phosphatidyl inositol 3-kinase (PI3K), Akt, and pAkt; the activity of the enzymes involved in glucose metabolism; and the levels of inflammatory cytokines.

resultsInsulin resistance was successfully induced in HepG2 cells. After treatment with AME, the glucose consumption increased significantly in HepG2 cells compared with the model group (MG). The expression of PI3K, Akt, and pAkt and the activity of 6-phosphofructokinas (PFK-1), glucokinase (GCK), and pyruvate kinase (PK) increased, while the activity of glycogen synthase kinase-3 (GSK-3), phosphoenolpyruvate carboxylase kinase (PEPCK), and glucose-6-phosphatase (G-6-Pase) as well as the levels of interleukin-6 (IL-6), interleukin-8 (IL-8), tumor necrosis factor-α (TNF-α), and C reactive protein (CRP) decreased.

conclusionsThe mechanism by which treatment with AME improves insulin resistance in HepG2 cells may involve the PI3K-Akt signaling pathway, the processes of glucose oxygenolysis, glycogen synthesis, gluconeogenesis and inflammatory cytokine expression.

Indexed as

BiflavonoidsCarcinoma, HepatocellularGene Expression Regulation, NeoplasticGlucoseGlycogen Synthase Kinase 3Hep G2 CellsHumansInsulinInsulin ResistanceInterleukin-6Interleukin-8Liver NeoplasmsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionTumor Necrosis Factor-alphaAKT1 protein, humanamentoflavoneBiflavonoidsCXCL8 protein, humanGlucoseGlycogen Synthase Kinase 3IL6 protein, humanInsulinInterleukin-6Interleukin-8Phosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTumor Necrosis Factor-alphaAMEglucose metabolisminflammatory cytokinesinsulin resistancePI3K-Akt

Identifiers

PMID27187341
PMCPMC6274486
OpenAlexW2386463695

What Socratic 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 Socratic graph.