ArticleInternational journal of molecular sciences2021
Chronic Treatment of Ascorbic Acid Leads to Age-Dependent Neuroprotection against Oxidative Injury in Hippocampal Slice Cultures.
Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- Association between dietary inflammatory potential and cognitive performance in children.European journal of nutrition · 2026Article
- Effect of Ascorbic Acid on the TransgenicCurrent Alzheimer research · 2026Article
- Article
- Role of Nanoparticle-Conjugates and Nanotheranostics in Abrogating Oxidative Stress and Ameliorating Neuroinflammation.Antioxidants (Basel, Switzerland) · 2023Review
- Antioxidant Therapy in Oxidative Stress-Induced Neurodegenerative Diseases: Role of Nanoparticle-Based Drug Delivery Systems in Clinical Translation.Antioxidants (Basel, Switzerland) · 2022Review
- Crosstalk between Neuron and Glial Cells in Oxidative Injury and Neuroprotection.International journal of molecular sciences · 2021Review
- Neuroprotection: Rescue from Neuronal Death in the Brain.International journal of molecular sciences · 2021Article
- Oxidative Stress and Cognitive Decline: The Neuroprotective Role of Natural Antioxidants.Frontiers in neuroscience · 2021Review
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Increased oxidative damage in the brain, which increases with age, is the cause of abnormal brain function and various diseases. Ascorbic acid (AA) is known as an endogenous antioxidant that provides neuronal protection against oxidative damage. However, with aging, its extracellular concentrations and uptake decrease in the brain. Few studies have dealt with age-related functional changes in the brain to sustained ascorbate supplementation. This study aimed to investigate the susceptibility of hippocampal neurons to oxidative injury following acute and chronic AA administration. Oxidative stress was induced by kainic acid (KA, 5 µM) for 18 h in hippocampal slice cultures. After KA exposure, less neuronal cell death was observed in the 3 w cultured slice compared to the 9 w cultured slice. In the chronic AA treatment (6 w), the 9 w-daily group showed reduced neuronal cell death and increased superoxide dismutase (SOD) and Nrf2 expressions compared to the 9 w. In addition, the 9 w group showed delayed latencies and reduced signal activity compared to the 3 w, while the 9 w-daily group showed shorter latencies and increased signal activity than the 9 w. These results suggest that the maintenance of the antioxidant system by chronic AA treatment during aging could preserve redox capacity to protect hippocampal neurons from age-related oxidative stress.
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Registered trials
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