ArticleInternational journal of molecular sciences2025
Bioactivity and Neuroprotective Effects of Extra Virgin Olive Oil in a Mouse Model of Cerebral Ischemia: An In Vitro and In Vivo Study.
Article in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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.
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Who cites it
2 citing papers in PubMed.
- Beneficial Effects of Olive Oil and the Mediterranean Diet on Alzheimer's Disease and Vascular Dementia: A Review.Medicina (Kaunas, Lithuania) · 2026Review
- Do different lipid emulsions affect brain development? A single-center retrospective analysis.Frontiers in nutrition · 2026Article
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Authors and funding
13 authors.
Funding
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Abstract
Cerebral ischemia is a pathological condition characterized by complete blood and oxygen supply deprivation to neuronal tissue. The ischemic brain compensates for the rapid decline in ATP levels by increasing the anaerobic glycolysis rate, which leads to lactate accumulation and subsequent acidosis. Astrocytes play a critical role in regulating cerebral energy metabolism. Mitochondria are significant targets in hypoxia-ischemia injury, and disruptions in mitochondrial homeostasis and cellular energetics worsen outcomes, especially in the elderly. Elevated levels of n-3 polyunsaturated fatty acids (PUFAs) protect the adult and neonatal brain from ischemic damage by suppressing inflammation, countering oxidative stress, supporting neurovascular unit reconstruction, and promoting oligodendrogenesis. This study examines extra virgin olive oil (EVOO) treatment on TNC WT and TNC M23 cells, focusing on oxygen consumption and reactive oxygen species (ROS) production. This study investigates the effects of different durations of middle cerebral artery occlusion (MCAo) and EVOO administration on cerebral infarct volume, neurological scores, mitochondrial function, and cell viability. Cerebral infarct volume increased with longer ischemia times, while EVOO treatment (0.5 mg/kg/day) significantly reduced infarction across all MCAo durations. The oxygen consumption assays demonstrate EVOO's dose-dependent stimulation of mitochondrial respiration in astrocytes, particularly at lower concentrations. Furthermore, EVOO-treated cells reduce ROS production during hypoxia, improve cell viability under ischemic stress, and enhance ATP production in ischemic conditions, underscoring EVOO's neuroprotective potential.
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