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Increased Superoxide Dismutase 2 by Allopregnanolone Ameliorates ROS-Mediated Neuronal Death in Mice with Pilocarpine-Induced Status Epilepticus

Authors
 Inja Cho  ;  Won-Joo Kim  ;  Hyun-Woo Kim  ;  Kyoung Heo  ;  Byung In Lee  ;  Yang-Je Cho 
Citation
 Neurochemical Research, Vol.43(7) : 1464-1475, 2018 
Journal Title
 Neurochemical Research 
ISSN
 0364-3190 
Issue Date
2018
MeSH
Animals ; Dose-Response Relationship, Drug ; Male ; Mice ; Mice, Inbred C57BL ; Pilocarpine/toxicity* ; Pregnanolone/pharmacology* ; Pregnanolone/therapeutic use ; Reactive Oxygen Species/metabolism* ; Status Epilepticus/chemically induced ; Status Epilepticus/metabolism* ; Status Epilepticus/prevention & control* ; Superoxide Dismutase/biosynthesis*
Keywords
Allopregnanolone ; Hippocampus ; Oxidative stress ; Status epilepticus ; Superoxide dismutase
Abstract
Excessive production of reactive oxygen species (ROS), along with dysfunction of the antioxidant defense system, such as that involving superoxide dismutase (SOD), may play a major role in neuronal death following status epilepticus (SE). Neurosteroids, which are allosteric modulators of the GABAA receptor in cerebral metabolism, have been suggested as being neuroprotective in various animal models; however, their effect to preventing ROS has not been examined. Herein, we investigate the neuroprotective role of allopregnanolone, the prototypical neurosteroid in the brain, in relation to the ROS-mediated neuronal injury. Adult male C57BL/6 mice were subjected to SE and treated with allopregnanolone. Hippocampal cell death was assessed by the terminal deoxynucleotidyl transferase dUTP nick end labeling assay, and ROS production was investigated by in situ detection of oxidized hydroethidine. SOD2 expression was analyzed by both western blot and immunofluorescent staining in the hippocampal subfields. In mice treated with allopregnanolone after SE, hippocampal cell death, DNA fragmentation, oxidative DNA damage, and ROS production were reduced significantly compared to mice subjected to vehicle treatment after SE. Hippocampal SOD2 expression was significantly increased by allopregnanolone. These finding suggest that allopregnanolone plays a neuroprotective role, with not only anticonvulsant but also antioxidant effects, by increasing SOD2 in pilocarpine-induced SE model.
Full Text
https://link.springer.com/article/10.1007%2Fs11064-018-2561-4
DOI
10.1007/s11064-018-2561-4
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Neurology (신경과학교실) > 1. Journal Papers
Yonsei Authors
김원주(Kim, Won Joo) ORCID logo https://orcid.org/0000-0002-5850-010X
조양제(Cho, Yang Je)
허경(Heo, Kyoung)
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URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/163735
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