ArticleMolecular neurobiology2025
Grape Seed Extract Pretreatment Prevents Mitochondrial Dysfunction and NLRP3 Inflammasome-Induced Inflammatory Response in Glial Cells Exposed to Paroxetine and Quinolinic Acid.
Article in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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Who cites it
2 citing papers in PubMed.
- Metabolic Reprogramming of Microglia in Neuroinflammation and Depression.International journal of molecular sciences · 2026Review
- Protective Effects of Ozone against Quinolinic Acid-Induced Redox Imbalance in Murine BV-2 Microglial Cells.Neurotoxicity research · 2026Article
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Depression is a neuropsychiatric disorder that affects thousands of people around the world. Drug therapy is the main approach for treating this disease, but its use can cause side effects on cells. This study aimed to examine the impact of antidepressant drugs from different classes on glial (BV-2) cells in the presence or absence of grape seed extract (GSE) and quinolinic acid (QA; 1.5 mM). Cells were treated with GSE (50 μg/mL; 23 h) and then exposed to non-cytotoxic concentrations of bupropion, imipramine, paroxetine, trazodone, and venlafaxine (27-181 µM; 1 h). Principal Component Analysis (PCA) was conducted to demonstrate the best combination of drug and extract treatment. Cell viability, adenosine triphosphate (ATP) production, reactive oxygen species (ROS) and nitric oxide (NO) levels, oxidative damage to lipids (TBARS), superoxide dismutase (SOD) activity, apoptosis, and NLR family pyrin domain containing 3 (NLRP3) genetic expression were evaluated by spectrophotometry, qRT-PCR, or flow cytometry. Mitochondrial markers (CI: NADH-CoQ reductase and CIV: cytochrome c oxidase) were also studied. GSE prevented the increment in levels of ROS (13.73-72.11%), TBARS (44.1-92.77%), NO (9.5-16%), SOD (68.44-212.29%) activity, and apoptosis (10.06-17.3%) caused by antidepressant drugs. Furthermore, it prevented impairments in complexes I (22-71.5%) and IV (7.5-92.5%) activities and ATP production (8-46%). GSE also prevented the NLRP3 overexpression in BV-2 activated by QA (62%), and paroxetine (46%), defined by PCA. Our study evidences that GSE can restore redox equilibrium and prevent inflammation caused by antidepressants and/or QA in a glial microenvironment.
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Registered trials
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