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© 2022 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.

Abstract

Astaxanthin is a powerful biological antioxidant and is naturally generated in a great variety of living organisms. Some studies have demonstrated the neuroprotective effects of ATX against ischemic brain injury in experimental animals. However, it is still unknown whether astaxanthin displays neuroprotective effects against severe ischemic brain injury induced by longer (severe) transient ischemia in the forebrain. The purpose of this study was to evaluate the neuroprotective effects of astaxanthin and its antioxidant activity in the hippocampus of gerbils subjected to 15-min transient forebrain ischemia, which led to the massive loss (death) of pyramidal cells located in hippocampal cornu Ammonis 1-3 (CA1-3) subfields. Astaxanthin (100 mg/kg) was administered once daily for three days before the induction of transient ischemia. Treatment with astaxanthin significantly attenuated the ischemia-induced loss of pyramidal cells in CA1-3. In addition, treatment with astaxanthin significantly reduced ischemia-induced oxidative DNA damage and lipid peroxidation in CA1-3 pyramidal cells. Moreover, the expression of the antioxidant enzymes superoxide dismutase (SOD1 and SOD2) in CA1-3 pyramidal cells were gradually and significantly reduced after ischemia. However, in astaxanthin-treated gerbils, the expression of SOD1 and SOD2 was significantly high compared to in-vehicle-treated gerbils before and after ischemia induction. Collectively, these findings indicate that pretreatment with astaxanthin could attenuate severe ischemic brain injury induced by 15-min transient forebrain ischemia, which may be closely associated with the decrease in oxidative stress due to astaxanthin pretreatment.

Details

Title
Astaxanthin Confers a Significant Attenuation of Hippocampal Neuronal Loss Induced by Severe Ischemia-Reperfusion Injury in Gerbils by Reducing Oxidative Stress
Author
Joon Ha Park 1 ; Lee, Tae-Kyeong 2 ; Kim, Dae Won 3   VIAFID ORCID Logo  ; Ahn, Ji Hyeon 4 ; Choong-Hyun, Lee 5   VIAFID ORCID Logo  ; Jong-Dai, Kim 6 ; Shin, Myoung Cheol 7 ; Cho, Jun Hwi 7 ; Lee, Jae-Chul 8 ; Moo-Ho, Won 8   VIAFID ORCID Logo  ; Soo Young Choi 9 

 Department of Anatomy, College of Korean Medicine, Dongguk University, Gyeongju 38066, Korea; [email protected] 
 Department of Food Science and Nutrition, Hallym University, Chuncheon 24252, Korea; [email protected] 
 Department of Biochemistry and Molecular Biology, Research Institute of Oral Sciences, College of Dentistry, Gangnung-Wonju National University, Gangneung 25457, Korea; [email protected] 
 Department of Physical Therapy, College of Health Science, Youngsan University, Yangsan 50510, Korea; [email protected] 
 Department of Pharmacy, College of Pharmacy, Dankook University, Cheonan 31116, Korea; [email protected] 
 Division of Food Biotechnology, School of Biotechnology, Kangwon National University, Chuncheon 24341, Korea; [email protected] 
 Department of Emergency Medicine, Kangwon National University Hospital, School of Medicine, Kangwon National University, Chuncheon 24289, Korea; [email protected] (M.C.S.); [email protected] (J.H.C.) 
 Department of Neurobiology, School of Medicine, Kangwon National University, Chuncheon 24341, Korea; [email protected] 
 Department of Biomedical Science and Research Institute for Bioscience and Biotechnology, Hallym University, Chuncheon 24252, Korea 
First page
267
Publication year
2022
Publication date
2022
Publisher
MDPI AG
e-ISSN
16603397
Source type
Scholarly Journal
Language of publication
English
ProQuest document ID
2653004850
Copyright
© 2022 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.