ArticleCurrent computer-aided drug design2025
Berberine Ameliorates High-fat-induced Insulin Resistance in HepG2 Cells by Modulating PPARs Signaling Pathway.
Article in Current computer-aided drug design, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Berberine: A Rising Star in the Management of Type 2 Diabetes-Novel Insights into Its Anti-Inflammatory, Metabolic, and Epigenetic Mechanisms.Pharmaceuticals (Basel, Switzerland) · 2025Review
- UPLC-Q-TOF-MS and network pharmacology to reveal the mechanism of Guizhi Gegen decoction against type 2 diabetes mellitus.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- NDUFAB1 as a Novel Regulator of NEFA-Induced Metabolic Dysfunction in Bovine Adipocytes.Animals : an open access journal from MDPI · 2025Article
- Pharmacokinetics Study of Herb-Drug Interaction ofInternational journal of analytical chemistry · 2025Article
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Authors and funding
7 authors.
Funding
Abstract
backgroundBerberine (BBR), also known as berberine hydrochloride, was isolated from the rhizomes of the Coptis chinensis. Studies have reported that BBR plays an important role in glycolipid metabolism, including insulin resistance (IR). The targets, and molecular mechanisms of BBR against hyperlipid-induced IR is worthy to be further studied. MATERIALS AND
methodsThe related targets of BBR were identified via Pharmmapper database and relevant targets of diabetes were obtained through GeneCards and Online Mendelian Inheritance in Man (OMIM) database. The common targets were employed with the STRING database and visualized with the protein-protein interactions (PPI) network. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis was performed to explore the biological progress and pathways.
results262 overlapped targets were extracted from BBR and diabetes. In the KEGG enrichment analysis, the peroxisome proliferator activated receptor (PPAR) signaling pathway was included. In vitro experiments, BBR can significantly increase sugar consumption and uptake in IR HepG2 cells, while PPAR inhibitors can weaken the effect of BBR on IR-HepG2.
conclusionThe PPAR signaling pathway is one of the important pathways for BBR to improve high-fat-induced insulin resistance in HepG2 cells.
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