Exp Neurobiol.  2015 Mar;24(1):41-54. 10.5607/en.2015.24.1.41.

Dehydroascorbic Acid Attenuates Ischemic Brain Edema and Neurotoxicity in Cerebral Ischemia: An in vivo Study

Affiliations
  • 1Department of Anatomy, Yonsei University College of Medicine, Seoul 120-752, Korea. jelee@yuhs.ac
  • 2BK21 Plus Project for Medical Sciences, and Brain Research Institute, Yonsei University College of Medicine, Seoul 120-752, Korea.
  • 3Department of Neurology, Seoul National University College of Medicine, Seoul 120-752, Korea.

Abstract

Ischemic stroke results in the diverse phathophysiologies including blood brain barrier (BBB) disruption, brain edema, neuronal cell death, and synaptic loss in brain. Vitamin C has known as the potent anti-oxidant having multiple functions in various organs, as well as in brain. Dehydroascorbic acid (DHA) as the oxidized form of ascorbic acid (AA) acts as a cellular protector against oxidative stress and easily enters into the brain compared to AA. To determine the role of DHA on edema formation, neuronal cell death, and synaptic dysfunction following cerebral ischemia, we investigated the infarct size of ischemic brain tissue and measured the expression of aquaporin 1 (AQP-1) as the water channel protein. We also examined the expression of claudin 5 for confirming the BBB breakdown, and the expression of bcl 2 associated X protein (Bax), caspase-3, inducible nitric oxide synthase (iNOS) for checking the effect of DHA on the neurotoxicity. Finally, we examined postsynaptic density protein-95 (PSD-95) expression to confirm the effect of DHA on synaptic dysfunction following ischemic stroke. Based on our findings, we propose that DHA might alleviate the pathogenesis of ischemic brain injury by attenuating edema, neuronal loss, and by improving synaptic connection.

Keyword

Dehydroascorbic acid (DHA); Cerebral ischemia; Edema; Blood-brain barrier (BBB); Neurotoxicity; Synaptic dysfunction

MeSH Terms

Aquaporins
Aquaporin 1
Ascorbic Acid
bcl-2-Associated X Protein
Blood-Brain Barrier
Brain
Brain Edema*
Brain Injuries
Brain Ischemia*
Caspase 3
Cell Death
Claudin-5
Dehydroascorbic Acid*
Edema
Neurons
Nitric Oxide Synthase Type II
Oxidative Stress
Post-Synaptic Density
Stroke
Aquaporins
Aquaporin 1
Ascorbic Acid
Caspase 3
Claudin-5
Dehydroascorbic Acid
Nitric Oxide Synthase Type II
bcl-2-Associated X Protein
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