ArticleNaunyn-Schmiedeberg's archives of pharmacology2026
Malvidin-3,5-O-diglucoside derived from spine grape (Vitis davidii) inhibits fructose-induced lipid accumulation in HepG2 cells: beneficial effects on MASLD treatment.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper, 1 of them a synthesis that pooled 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.
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.
Who cites it
1 citing paper in PubMed, 1 synthesis or guideline pooled it.
- Hepato-Renal Axis: A Systematic Review of Anthocyanin Protective Mechanisms of Preclinical Evidence.Molecular nutrition & food research · 2026Pooled it
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
Metabolic dysfunction-associated steatotic liver disease (MASLD) is considered an important independent risk factor for hepatocellular carcinoma. This study aims to investigate the anti-lipogenic effects and mechanisms of Malvidin-3,5-O-diglucoside (M35G) derived from Vitis davidii on a high-fructose-induced MASLD cell model in HepG2 cells. Through the detection of various physicochemical indicators, histology, free fatty acids and their metabolites, transcription factors, and enzyme expression, it was demonstrated that 10 mM fructose treatment for 72 h significantly increased lipid accumulation in HepG2 cells. M35G reduced hepatic lipid accumulation and improves free fatty acids metabolism by inhibiting the expression of transcription factors and enzymes involved in de novo lipogenesis and promoting the β-oxidation of fatty acids. M35G also ameliorated fructose-induced glucose metabolism disorder by suppressing ketohexokinase-c and phosphoenolpyruvate carboxykinase expression while upregulating adenosine 5'-monophosphate-activated protein kinase and pyruvate kinase M2 isoform expression. This validated the inhibitory role of M35G in mediating the development of fatty liver disease, which may aid in the prevention and treatment of MASLD.
Indexed as
Identifiers
41152612What Socratic holds
Registered trials
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.