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Pretreatment of Populus tomentiglandulosa protects hippocampal CA1 pyramidal neurons from ischemia-reperfusion injury in gerbils via increasing SODs expressions and maintaining BDNF and IGF-I expressions.

Identifieur interne : 000814 ( Main/Corpus ); précédent : 000813; suivant : 000815

Pretreatment of Populus tomentiglandulosa protects hippocampal CA1 pyramidal neurons from ischemia-reperfusion injury in gerbils via increasing SODs expressions and maintaining BDNF and IGF-I expressions.

Auteurs : Tae-Kyeong Lee ; Joon Ha Park ; Ji Hyeon Ahn ; Hyunjung Kim ; Minah Song ; Jae-Chul Lee ; Jong Dai Kim ; Yong Hwan Jeon ; Jung Hoon Choi ; Choong Hyun Lee ; In Koo Hwang ; Bing-Chun Yan ; Moo-Ho Won ; Il Jun Kang

Source :

RBID : pubmed:31262455

English descriptors

Abstract

To examine the effects of Populus tomentiglandulosa (PT) extract on the expressions of antioxidant enzymes and neurotrophic factors in the cornu ammonis 1 (CA1) region of the hippocampus at 5 min after inducing transient global cerebral ischemia (TGCI) in gerbils, TGCI was induced by occlusion of common carotid arteries for 5 min. Before ischemic surgery, 200 mg·kg-1 PT extract was orally administrated once daily for 7 d. We performed neuronal nuclear antigen immunohistochemistry and Fluoro-Jade B staining. Furthermore, we determined in situ production of superoxide anion radical, expression levels of SOD1 and SOD2 as antioxidant enzymes and brain-derived neurotrophic factor (BDNF) and insulin-like growth factor I (IGF-I) as neurotrophic factors. Pretreatment with 200 mg·kg-1 PT extract prevented neuronal death (loss). Furthermore, pretreatment with 200 mg·kg-1 PT extract significantly inhibited the production of superoxide anion radical, increased expressions of SODs and maintained expressions of BDNF and IGF-I. Such increased expressions of SODs were maintained in the neurons after IRI. In summary, pretreated PT extract can significantly increase levels of SODs and protect the neurons against TGCI, suggesting that PT can be a useful natural agent to protect against TGCI.

DOI: 10.1016/S1875-5364(19)30050-0
PubMed: 31262455

Links to Exploration step

pubmed:31262455

Le document en format XML

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<term>Animals (MeSH)</term>
<term>Brain-Derived Neurotrophic Factor (genetics)</term>
<term>Brain-Derived Neurotrophic Factor (metabolism)</term>
<term>CA1 Region, Hippocampal (drug effects)</term>
<term>CA1 Region, Hippocampal (metabolism)</term>
<term>Gerbillinae (MeSH)</term>
<term>Humans (MeSH)</term>
<term>Insulin-Like Growth Factor I (genetics)</term>
<term>Insulin-Like Growth Factor I (metabolism)</term>
<term>Male (MeSH)</term>
<term>Neuroprotective Agents (administration & dosage)</term>
<term>Plant Extracts (administration & dosage)</term>
<term>Populus (chemistry)</term>
<term>Pyramidal Cells (drug effects)</term>
<term>Pyramidal Cells (metabolism)</term>
<term>Reperfusion Injury (drug therapy)</term>
<term>Reperfusion Injury (genetics)</term>
<term>Reperfusion Injury (metabolism)</term>
<term>Superoxide Dismutase (genetics)</term>
<term>Superoxide Dismutase (metabolism)</term>
<term>Up-Regulation (drug effects)</term>
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<keywords scheme="MESH" type="chemical" qualifier="administration & dosage" xml:lang="en">
<term>Neuroprotective Agents</term>
<term>Plant Extracts</term>
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<term>Brain-Derived Neurotrophic Factor</term>
<term>Insulin-Like Growth Factor I</term>
<term>Superoxide Dismutase</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en">
<term>Brain-Derived Neurotrophic Factor</term>
<term>Insulin-Like Growth Factor I</term>
<term>Superoxide Dismutase</term>
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<term>Populus</term>
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<keywords scheme="MESH" qualifier="drug effects" xml:lang="en">
<term>CA1 Region, Hippocampal</term>
<term>Pyramidal Cells</term>
<term>Up-Regulation</term>
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<term>Reperfusion Injury</term>
</keywords>
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<term>Reperfusion Injury</term>
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<term>Reperfusion Injury</term>
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<div type="abstract" xml:lang="en">To examine the effects of Populus tomentiglandulosa (PT) extract on the expressions of antioxidant enzymes and neurotrophic factors in the cornu ammonis 1 (CA1) region of the hippocampus at 5 min after inducing transient global cerebral ischemia (TGCI) in gerbils, TGCI was induced by occlusion of common carotid arteries for 5 min. Before ischemic surgery, 200 mg·kg
<sup>-1</sup>
PT extract was orally administrated once daily for 7 d. We performed neuronal nuclear antigen immunohistochemistry and Fluoro-Jade B staining. Furthermore, we determined in situ production of superoxide anion radical, expression levels of SOD1 and SOD2 as antioxidant enzymes and brain-derived neurotrophic factor (BDNF) and insulin-like growth factor I (IGF-I) as neurotrophic factors. Pretreatment with 200 mg·kg
<sup>-1</sup>
PT extract prevented neuronal death (loss). Furthermore, pretreatment with 200 mg·kg
<sup>-1</sup>
PT extract significantly inhibited the production of superoxide anion radical, increased expressions of SODs and maintained expressions of BDNF and IGF-I. Such increased expressions of SODs were maintained in the neurons after IRI. In summary, pretreated PT extract can significantly increase levels of SODs and protect the neurons against TGCI, suggesting that PT can be a useful natural agent to protect against TGCI.</div>
</front>
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<AbstractText>To examine the effects of Populus tomentiglandulosa (PT) extract on the expressions of antioxidant enzymes and neurotrophic factors in the cornu ammonis 1 (CA1) region of the hippocampus at 5 min after inducing transient global cerebral ischemia (TGCI) in gerbils, TGCI was induced by occlusion of common carotid arteries for 5 min. Before ischemic surgery, 200 mg·kg
<sup>-1</sup>
PT extract was orally administrated once daily for 7 d. We performed neuronal nuclear antigen immunohistochemistry and Fluoro-Jade B staining. Furthermore, we determined in situ production of superoxide anion radical, expression levels of SOD1 and SOD2 as antioxidant enzymes and brain-derived neurotrophic factor (BDNF) and insulin-like growth factor I (IGF-I) as neurotrophic factors. Pretreatment with 200 mg·kg
<sup>-1</sup>
PT extract prevented neuronal death (loss). Furthermore, pretreatment with 200 mg·kg
<sup>-1</sup>
PT extract significantly inhibited the production of superoxide anion radical, increased expressions of SODs and maintained expressions of BDNF and IGF-I. Such increased expressions of SODs were maintained in the neurons after IRI. In summary, pretreated PT extract can significantly increase levels of SODs and protect the neurons against TGCI, suggesting that PT can be a useful natural agent to protect against TGCI.</AbstractText>
<CopyrightInformation>Copyright © 2019 China Pharmaceutical University. Published by Elsevier B.V. All rights reserved.</CopyrightInformation>
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<ForeName>Choong Hyun</ForeName>
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<LastName>Yan</LastName>
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<Affiliation>Department of Neurobiology, School of Medicine, Kangwon National University, Chuncheon 24341, Republic of Korea. Electronic address: mhwon@kangwon.ac.kr.</Affiliation>
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</Author>
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<LastName>Kang</LastName>
<ForeName>Il Jun</ForeName>
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<Affiliation>Department of Food Science and Nutrition, Hallym University, Chuncheon 24252, Republic of Korea. Electronic address: ijkang@hallym.ac.kr.</Affiliation>
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   |texte=   Pretreatment of Populus tomentiglandulosa protects hippocampal CA1 pyramidal neurons from ischemia-reperfusion injury in gerbils via increasing SODs expressions and maintaining BDNF and IGF-I expressions.
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