Dehydroascorbic Acid Attenuates Ischemic Brain Edema and Neurotoxicity in Cerebral Ischemia: An in vivo Study.
- Author:
Juhyun SONG
1
;
Joohyun PARK
;
Jae Hwan KIM
;
Ja Yong CHOI
;
Jae Young KIM
;
Kyoung Min LEE
;
Jong Eun LEE
Author Information
- Publication Type:Original Article
- Keywords: Dehydroascorbic acid (DHA); Cerebral ischemia; Edema; Blood-brain barrier (BBB); Neurotoxicity; Synaptic dysfunction
- MeSH: 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
- From:Experimental Neurobiology 2015;24(1):41-54
- CountryRepublic of Korea
- Language:English
- 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.
