ArticleBiomolecules2020
Pharmaceutical Efficacy of Gypenoside LXXV on Non-Alcoholic Steatohepatitis (NASH).
Article in Biomolecules, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 2 of them syntheses that pooled it.
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Who cites it
15 citing papers in PubMed, 2 syntheses or guidelines pooled it, 24 citations in OpenAlex.
- Novel insights from meta-analysis: the efficacy of ginsenosides in non-alcoholic fatty liver disease.Frontiers in pharmacology · 2025Pooled it
- The Efficacy ofNutrients · 2023Pooled it
- Secondary Metabolites from a New Antibiotic-Producing Endophytic Streptomyces Isolate Inhibited Pathogenic and Multidrug-ResistantTropical medicine and infectious disease · 2025Article
- Molecular mechanisms behind the inhibitory effects of ginsenoside Rg3 on hepatic fibrosis: a review.Archives of toxicology · 2025Review
- [Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2025Article
- Gypenosides, a promising phytochemical triterpenoid: research progress on its pharmacological activity and mechanism.Frontiers in pharmacology · 2025Review
- The Active Components of Traditional Chinese Medicines Regulate the Multi-Target Signaling Pathways of Metabolic Dysfunction-Associated Fatty Liver Disease.Drug design, development and therapy · 2025Review
- A Review of the Therapeutic Potential of Ginseng and Its Bioactive Components in Nonalcoholic Fatty Liver Disease.Drug design, development and therapy · 2025Review
- Article
- Gypenoside XIII regulates lipid metabolism in HepG2 hepatocytes and ameliorates nonalcoholic steatohepatitis in mice.The Kaohsiung journal of medical sciences · 2024Article
- The pharmacological role of Ginsenoside Rg3 in liver diseases: A review on molecular mechanisms.Journal of ginseng research · 2024Review
- 6-Shogaol Ameliorates Liver Inflammation and Fibrosis in Mice on a Methionine- and Choline-Deficient Diet by Inhibiting Oxidative Stress, Cell Death, and Endoplasmic Reticulum Stress.Molecules (Basel, Switzerland) · 2024Article
- Article
- Pharmacological properties, molecular mechanisms and therapeutic potential of ginsenoside Rg3 as an antioxidant and anti-inflammatory agent.Frontiers in pharmacology · 2022Review
- Identification and chemical profiling of anti-alcoholic liver disease biomarkers of ginseng Huang jiu using UPLC-Q-Orbitrap-HRMS and network pharmacology-based analyses.Frontiers in nutrition · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ginsenosides have offered a wide array of beneficial roles in the pharmacological regulation of hepatic metabolic syndromes, including non-alcoholic steatohepatitis (NASH), non-alcoholic fatty liver disease (NAFLD), and obesity. Of the numerous ginsenosides, Rg3 has been widely investigated, but there have been few studies of gypenosides (Gyp). Particularly, no study on Gyp LXXV has been reported to date. Here, to firstly explore the pharmacological effects of Gyp LXXV against NASH and the related mechanism, methionine- and choline-deficient (MCD) diet-induced NASH mice and hepatic cells (stellate cells, hepatic macrophages, and hepatocytes) were selected. Gyp LXXV exhibited markedly alleviated MCD diet-induced hepatic injury, inflammation, and fibrosis by down-regulating hepatic fibrosis markers such as α-smooth muscle actin(α-SMA), collagen1, transforming growth factors-β (TGF-β1), tumor necrosis factor-α (TNF-α), MCP-1, interleukin (IL)-1β, nuclear factor κB (NFκB), and GRP78. Remarkably, histopathological studies confirmed that 15 mg/kg of Gyp LXXV administration to MCD diet-induced mice led to effective prevention of liver injury, lipid accumulation, and activation of hepatic macrophages, indicating that Gyp LXXV might be a potential anti-NASH drug.
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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.