ArticleBMC complementary medicine and therapies2023
Gallic acid and metformin co-administration reduce oxidative stress, apoptosis and inflammation via Fas/caspase-3 and NF-κB signaling pathways in thioacetamide-induced acute hepatic encephalopathy in rats.
Article in BMC complementary medicine and therapies, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 24 citations in OpenAlex.
- Liraglutide Attenuates Multiorgan Oxidative, Astroglial, and Mitochondrial Stress Responses in Thioacetamide-Induced Hepatic Encephalopathy.International journal of molecular sciences · 2026Article
- Encephalopathy: Cause, Pathogenesis, and Treatment.MedComm · 2026Review
- Oleuropein modulates behavioral changes, apoptosis, autophagy, inflammation, oxidative stress-associated PI3K/Akt/mTOR pathways in TAA-Induced hepatic encephalopathy.Metabolic brain disease · 2026Article
- Mechanistic pathways andIranian journal of basic medical sciences · 2026Article
- Lemon Juice-Assisted Green Extraction of Strawberry Enhances Neuroprotective Phytochemicals: Insights into Alzheimer's-Related Pathways.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Metformin Ameliorates Early Brain Injury After Subarachnoid Hemorrhage Via Improving Endoplasmic Reticulum Stress and Mitochondrial Stress-Mediated CaMolecular neurobiology · 2025Article
- The Protective Effect of Phenolic Acids on Liver Disease: A Review of Possible Mechanisms.Antioxidants (Basel, Switzerland) · 2025Review
- The ameliorative effects of metformin and taurine against thioacetamide hepatotoxicity in rats.Toxicology research · 2025Article
- Treatment with hydrogen-rich water protects against thioacetamide-induced hepatic encephalopathy in rats through stabilizing liver-brain disturbance.Scientific reports · 2025Article
- HPLC-HRMS/MS and anti-inflammatory effects of bunya pine resin through multifaceted pathway modulation: NUMB/NOTCH1/HES1/mTOR/ PI3K/HMGB1 signaling cascades.Inflammopharmacology · 2025Article
- Gallic and glycyrrhetinic acids prevent azithromycin-induced liver damage in rats by mitigating oxidative stress and inflammation.Scientific reports · 2025Article
- Gallic acid alleviates exercise-induced muscle damage by inhibiting mitochondrial oxidative stress and ferroptosis.Journal of translational medicine · 2025Article
- The role of gallic acid in liver disease: a review of its phytochemistry, pharmacology, and safety.Frontiers in pharmacology · 2025Review
- Gallic acid ameliorates LPS-induced memory decline by modulating NF-κB, TNF-α, and Caspase 3 gene expression and attenuating oxidative stress and neuronal loss in the rat hippocampus.Metabolic brain disease · 2024Article
- Synergistic Effect of Flavonoids and Metformin on Protection of the Methylglyoxal-Induced Damage in PC-12 Neuroblastoma Cells: Structure-Activity Relationship and Potential Target.Molecules (Basel, Switzerland) · 2024Article
- A preliminary study on Tapyadi Loha for the treatment of hepatic encephalopathy based on Insilico and Invitro analysis.Journal of Ayurveda and integrative medicineArticle
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHepatic encephalopathy (HE) is a consequence of chronic or acute liver diseases. This study evaluates the combined effect of gallic acid (GA), and metformin (Met) on the liver and brain damage associated with HE.
methodsAcute HE was induced by a single dose of thioacetamide (TAA) (300 mg/kg) as an I.P. injection. Treated groups received GA group (100 mg/kg/day, p.o), Met (200 mg/kg/day, p.o), or their combination for 25 consecutive days before TAA injection.
resultsThe administration of TAA induced various biochemical and histopathological alterations. In contrast, treatment with GA either alone or combined with Met resulted in improved liver functions by the significant reduction in serum ALT, AST, and ALP activities, and ammonia levels. Inflammatory mediators; TNF-α, IL-6, and NFkβ levels were decreased by these treatments as well as apoptotic cascade via down-regulation of FAS and caspase-3 (CASP-3) expression in hepatic tissues. Furthermore, GA and Met either alone or combined protected the liver and brain tissues from damage by increased glutathione concentration while decreasing malondialdehyde. In addition, it was accompanied by the improvement of the brain neurotransmitter profile via the restoration of norepinephrine, dopamine, and serotonin levels. Based on our data, this is the first study to report a novel combined hepatoprotective and cognitive enhancing effect of GA and Met against TAA-induced acute liver and brain injury.
conclusionGA and Met combination resulted in a prominent improvement in HE complications, relative to monotherapy. Both agents potentiated the antioxidant, anti-inflammatory, and anti-apoptotic effects of each other.
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