ArticleMolecular medicine (Cambridge, Mass.)2024
Pentagalloylglucose alleviates acetaminophen-induced acute liver injury by modulating inflammation via cGAS-STING pathway.
Article in Molecular medicine (Cambridge, Mass.), 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.
- Recent progress in cGAS-STING agonist design and mechanisms of cancer immune modulation.RSC chemical biology · 2026Review
- Gut-liver axis molecular mechanisms in alcohol-associated liver disease.Alcohol (Fayetteville, N.Y.) · 2026Review
- Beyond Sensory Properties: Molecular Interactions of Antioxidant Flavour-Active Polyphenols Across the Food-Oral-Gut Axis.Antioxidants (Basel, Switzerland) · 2026Review
- Chestnut Tannin Improves Growth Performance and Intestinal Health of Broilers Challenged with Necrotic Enteritis via the cGAS-STING-Ferroptosis Pathway.Animals : an open access journal from MDPI · 2026Article
- Polyphenols ameliorate metabolic disorders by remodeling gut microbiota and regulating Nrf2/NF-κB signaling pathways.Frontiers in microbiology · 2026Review
- Response mechanism of hepatorenal metabolic barrier function to drugs and environmental poisons and intervention strategy of natural products.Frontiers in pharmacology · 2026Review
- Sophora tonkinensis enhances activation of cGAS-STING pathway and restrains HBV replication.Frontiers in pharmacology · 2025Article
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Authors and funding
13 authors.
Funding
Abstract
backgroundThe cGAS-STING pathway is an important component of the innate immune system and plays significant role in acetaminophen-induced liver injury (AILI). Pentagalloylglucose (PGG) is a natural polyphenolic compound with various beneficial effects, including anti-cancer, antioxidant, anti-inflammatory, and liver-protective properties; however, whether it can be used for the treatment of AILI and the specific mechanism remain unclear. MATERIALS AND
methodsA cell culture model was created to study the effect of PGG on cGAS-STING pathway activation using various techniques including western blotting (WB), real-time quantitative polymerase chain reaction (RT-qPCR), immunofluorescence (IF), and immunoprecipitation (IP). The effect of PGG was investigated in vivo by establishing a dimethylxanthenone acetic acid (DMXAA)-mediated activation model. An AILI model was used to evaluate the hepatoprotective and therapeutic effects of PGG by detecting liver function indicators, liver histopathology, and cGAS-STING pathway-related indicators in mice with AILI.
resultsPGG blocked cGAS-STING pathway activation in bone marrow-derived macrophages (BMDMs), THP-1 cells, and peripheral blood mononuclear cells (PBMCs) in vitro. Furthermore, PGG inhibited the generation of type I interferons (IFN-I) and the secretion of inflammatory factors in DMXAA-induced in vivo experiments. In addition, PGG also reduced serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP), improved liver tissue damage and apoptosis, and inhibited the cGAS-STING pathway activation caused by acetaminophen. In terms of the mechanism, PGG disrupted the connection between STING and TBK1.
conclusionsPGG exerts a protective effect against AILI by blocking the cGAS-STING pathway, offering a promising treatment strategy.
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