ArticleNutrients2014
Orally administrated ascorbic acid suppresses neuronal damage and modifies expression of SVCT2 and GLUT1 in the brain of diabetic rats with cerebral ischemia-reperfusion.
Article in Nutrients, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.
- Vitamin C Intake and Ischemic Stroke.Frontiers in nutrition · 2022Pooled it
- The Efficacy of Vitamin C on Postoperative Outcomes after Posterior Lumbar Interbody Fusion: A Randomized, Placebo-Controlled Trial.Clinics in orthopedic surgery · 2017Trial
- Administration of Ascorbic Acid Alleviates Neuronal Damage After Cerebral Ischemia in ODS Rats.Antioxidants (Basel, Switzerland) · 2025Article
- Possible role of vitamins C and E co-administration in the prevention of testicular ischemia-reperfusion injury following surgical repair of torsion of the testis.Frontiers in nutrition · 2025Review
- The protective role of endothelial GLUT1 in ischemic stroke.Brain and behavior · 2024Review
- Involvement of the Restoration of Cerebral Blood Flow and Maintenance of eNOS Expression in the Prophylactic Protective Effect of the Novel Ferulic Acid Derivative FAD012 against Ischemia/Reperfusion Injuries in Rats.International journal of molecular sciences · 2023Article
- Dimethyloxalylglycine pretreatment of living donor alleviates both donor and graft liver ischemia-reperfusion injury in rats.Frontiers in pharmacology · 2023Article
- High-Dose Vitamin C Prevents Secondary Brain Damage After Stroke via Epigenetic Reprogramming of Neuroprotective Genes.Translational stroke research · 2022Article
- Natural Antioxidant Evaluation: A Review of Detection Methods.Molecules (Basel, Switzerland) · 2022Review
- Involvement of glucose transporter overexpression in the protection or damage after ischemic stroke.Neural regeneration research · 2022Article
- Review
- Article
- Glucose transporters in brain in health and disease.Pflugers Archiv : European journal of physiology · 2020Review
- Pyrethroid-Induced Organ Toxicity and Anti-Oxidant-Supplemented Amelioration of Toxicity and Organ Damage: The Protective Roles of Ascorbic Acid and α-Tocopherol.International journal of environmental research and public health · 2020Article
- Effects of Vitamin C on the Prevention of Ischemia-Reperfusion Brain Injury: Experimental Study in Rats.International journal of vascular medicine · 2019Article
- Distinctive Neurochemistry in Alzheimer's Disease via 7 T In Vivo Magnetic Resonance Spectroscopy.Journal of Alzheimer's disease : JAD · 2019Article
- Conjugation to Ascorbic Acid Enhances Brain Availability of Losartan Carboxylic Acid and Protects Against Parkinsonism in Rats.The AAPS journal · 2018Article
- SVCT2 Expression and Function in Reactive Astrocytes Is a Common Event in Different Brain Pathologies.Molecular neurobiology · 2018Article
- Diabetic aggravation of stroke and animal models.Experimental neurology · 2017Review
- Dehydroascorbic Acid Attenuates Ischemic Brain Edema and Neurotoxicity in Cerebral Ischemia: An in vivo Study.Experimental neurobiology · 2015Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetes mellitus is known to exacerbate cerebral ischemic injury. In the present study, we investigated antiapoptotic and anti-inflammatory effects of oral supplementation of ascorbic acid (AA) on cerebral injury caused by middle cerebral artery occlusion and reperfusion (MCAO/Re) in rats with streptozotocin-induced diabetes. We also evaluated the effects of AA on expression of sodium-dependent vitamin C transporter 2 (SVCT2) and glucose transporter 1 (GLUT1) after MCAO/Re in the brain. The diabetic state markedly aggravated MCAO/Re-induced cerebral damage, as assessed by infarct volume and edema. Pretreatment with AA (100 mg/kg, p.o.) for two weeks significantly suppressed the exacerbation of damage in the brain of diabetic rats. AA also suppressed the production of superoxide radical, activation of caspase-3, and expression of proinflammatory cytokines (tumor necrosis factor-α and interleukin-1β) in the ischemic penumbra. Immunohistochemical staining revealed that expression of SVCT2 was upregulated primarily in neurons and capillary endothelial cells after MCAO/Re in the nondiabetic cortex, accompanied by an increase in total AA (AA + dehydroascorbic acid) in the tissue, and that these responses were suppressed in the diabetic rats. AA supplementation to the diabetic rats restored these responses to the levels of the nondiabetic rats. Furthermore, AA markedly upregulated the basal expression of GLUT1 in endothelial cells of nondiabetic and diabetic cortex, which did not affect total AA levels in the cortex. These results suggest that daily intake of AA attenuates the exacerbation of cerebral ischemic injury in a diabetic state, which may be attributed to anti-apoptotic and anti-inflammatory effects via the improvement of augmented oxidative stress in the brain. AA supplementation may protect endothelial function against the exacerbated ischemic oxidative injury in the diabetic state and improve AA transport through SVCT2 in the cortex.
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