Evidence map›Paper›PMID 37996895›Full record

ArticleNutrition & metabolism2023

Exploring the underlying mechanisms of fisetin in the treatment of hepatic insulin resistance via network pharmacology and in vitro validation.

Tian Li, Junjun Ling, Xingrong Du, Siyu Zhang, Yan Yang, Liang Zhang

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nutrition & metabolism, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

5 citing papers in PubMed, 10 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

6 authors at 4 institutions in 1 country.

Tian LiMetabilic Vascular Disease Key Laboratory of Sichuan Province, Luzhou, 646000, China.
Junjun LingAffiliated Hospital of Guizhou Medical University, Guiyang, 550000, China.
Xingrong DuMetabilic Vascular Disease Key Laboratory of Sichuan Province, Luzhou, 646000, China.
Siyu ZhangDrug Discovery Research Center, Southwest Medical University, Luzhou, 646000, China.
Yan YangChongqing Tongnan NO.1 Middle School, Tongnan, 402660, China.
Liang ZhangMetabilic Vascular Disease Key Laboratory of Sichuan Province, Luzhou, 646000, China. zhangliangsyd@163.com.
First Affiliated Hospital of Sichuan Medical University · CNGuiyang Medical University · CNSouthwest Medical University · CNUniversity of Electronic Science and Technology of China · CN

Funding

the Natural Science Foundation of Sichuan Province 2022NSFSC1601the Open Project Program of Metabolic Vascular Diseases Key Laboratory of Sichuan Province 2022MVDKL-G2
6 · The paper itself

Abstract

objectiveTo characterize potential mechanisms of fisetin on hepatic insulin resistance (IR) using network pharmacology and in vitro validation.

methodsPutative targets of fisetin were retrieved from the Traditional Chinese Medicine Systems Pharmacology database, whereas the potential genes of hepatic IR were obtained from GeneCards database. A protein-protein interaction (PPI) network was constructed according to the intersection targets of fisetin and hepatic IR using the Venn diagram. The biological functions and potential pathways related to genes were determined using Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses. Cell experiments were also conducted to further verify the mechanism of fisetin on hepatic IR.

resultsA total of 118 potential targets from fisetin were associated with hepatic IR. The areas of nodes and corresponding degree values of TP53, AKT1, TNF, IL6, CASP3, CTNNB1, JUN, SRC, epidermal growth factor receptor (EGFR), and HSP90AA1 were larger and could be easily found in the PPI network. Furthermore, GO analysis revealed that these key targets were significantly involved in multiple biological processes that participated in oxidative stress and serine/threonine kinase activity. KEGG enrichment analysis showed that the PI3K/AKT signaling pathway was a significant pathway involved in hepatic IR. Our in vitro results demonstrated that fisetin treatment increased the expressions of EGFR and IRS in HepG2 and L02 cells under normal or IR conditions. Western blot results revealed that p-AKT/AKT levels were significantly up-regulated, suggesting that fisetin was involved in the PI3K/AKT signaling pathway to regulate insulin signaling.

conclusionWe explored the pharmacological actions and the potential molecular mechanism of fisetin in treating hepatic IR from a holistic perspective. Our study lays a theoretical foundation for the development of fisetin for type 2 diabetes.

Indexed as

Epidermal growth factor receptorFisetinHepatic insulin resistanceNetwork pharmacologyPI3K/AKT signaling

Identifiers

PMID37996895
PMCPMC10666360
OpenAlexW4388943469

What Socratic 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 Socratic graph.