ArticleFrontiers in pharmacology2024
Gentiopicroside improves non-alcoholic steatohepatitis by activating PPARα and suppressing HIF1.
Article in Frontiers in pharmacology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 6 citations in OpenAlex.
- Molecular Mechanism of Dihydroquercetin in Ameliorating Metabolic Dysfunction-Associated Steatotic Liver Disease: Insights Into the HIF-1α/VEGF Pathway.Food science & nutrition · 2026Article
- Extract of camellia seed cake ameliorates glycolipid metabolism disorder in mice through inhibiting ACOX1 activity.Food chemistry: X · 2025Article
- [Curcumin inhibits lipid metabolism in non-small cell lung cancer by downregulating the HIF-1α pathway].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025Article
- Therapeutic efficacy and mechanisms of gentiopicroside in various diseases.Frontiers in pharmacology · 2025Review
- Effect of gentiopicroside on endogenous formaldehyde homocysteine-pathway related proteins in rats with non-alcoholic steatohepatitis.Frontiers in pharmacology · 2025Article
- Article
- Nitidine Chloride Alleviates Hypoxic Stress via PINK1-Parkin-Mediated Mitophagy in the Mammary Epithelial Cells of Milk Buffalo.Animals : an open access journal from MDPI · 2024Article
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Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gentiopicroside (GPS) is a highly water-soluble small-molecule drug and the main bioactive secoiridoid glycoside of Gentiana scabra that has been shown to have hepatoprotective effects against non-alcoholic steatohepatitis (NASH), a form of non-alcoholic fatty liver disease (NAFLD) that can progress to cirrhosis and hepatocellular carcinoma. However, the effects of GPS on NASH and the underlying mechanisms remain obscure. Firstly, a high-fat, high-cholesterol (HFHC) diet and a high-sugar solution containing d-fructose and d-glucose were used to establish a non-alcoholic steatohepatitis (NASH) mice model. Secondly, we confirmed GPS supplementation improve metabolic abnormalities and reduce inflammation in NASH mice induced by HFHC and high-sugar solution. Then we used metabolomics to investigate the mechanisms of GPS in NASH mice. Metabolomics analysis showed GPS may work through the Peroxisome Proliferator-Activated Receptor (PPAR) signaling pathway and glycine, serine, and threonine metabolism. Functional metabolites restored by GPS included serine, glycine, eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA). Western blot and qRT-PCR analysis confirmed GPS improve NASH by regulating PPARα and Hypoxia-Inducible Factor-1α (HIF-1α) signaling pathways.
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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.