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231226s2022 xx |||||o 00| ||eng c |
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|a 10.1155/2022/6509981
|2 doi
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|a pubmed25n1167.xml
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|a DE-627
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|e rakwb
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|a eng
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| 100 |
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|a Meng, Yan
|e verfasserin
|4 aut
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|a Astragaloside IV Alleviates Brain Injury Induced by Hypoxia via the Calpain-1 Signaling Pathway
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|c 2022
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|a Text
|b txt
|2 rdacontent
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|a ƒaComputermedien
|b c
|2 rdamedia
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|a ƒa Online-Ressource
|b cr
|2 rdacarrier
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|a Date Completed 14.12.2022
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|a Date Revised 08.09.2024
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|a published: Electronic-eCollection
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|a Citation Status MEDLINE
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|a Copyright © 2022 Yan Meng et al.
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|a Long-term hypoxia can induce oxidative stress and apoptosis in hippocampal neurons that can lead to brain injury diseases. Astragaloside IV (AS-IV) is widely used in the antiapoptotic therapy of brain injury diseases. However, its mechanism of action is still not fully understood. In this study, we investigated the effect of AS-IV on hypoxia-induced oxidative stress and apoptosis in hippocampal neurons and explored its possible mechanism. In vivo, mice were placed in a hypoxic circulatory device containing 10% O2 and gavaged with AS-IV (60 and 120 mg/kg/d) for 4 weeks. In vitro, mouse hippocampal neuronal cells (HT22) were treated with hypoxia (1% O2) for 24 hours in the presence or absence of AS-IV, MDL-28170 (calpain-1 inhibitor), or YC-1 (HIF-1α inhibitor). The protective effect of AS-IV on brain injury was further explored by examining calpain-1 knockout mice. The results showed that hypoxia induced damage to hippocampal neurons, impaired spatial learning and memory abilities, and increased oxidative stress and apoptosis. Treatment with AS-IV or calpain-1 knockout improved the damage to hippocampal neurons and spatial learning and memory, attenuated oxidative stress and inhibited cell apoptosis. These changes were verified in HT22 cells. Overexpression of calpain-1 abolished the improvement of AS-IV on apoptosis and oxidative stress. In addition, the effects of AS-IV were accompanied by decreased calpain-1 and HIF-1α expression, and YC-1 showed a similar effect as AS-IV on calpain-1 and caspase-3 expression. In conclusion, this study demonstrates that AS-IV can downregulate the calpain-1/HIF-1α/caspase-3 pathway and inhibit oxidative stress and apoptosis of hippocampal neurons induced by hypoxia, which provides new ideas for studying the antiapoptotic activity of AS-IV
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|a Journal Article
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|a Research Support, Non-U.S. Gov't
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|a astragaloside A
|2 NLM
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|a 3A592W8XKE
|2 NLM
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|a Caspase 3
|2 NLM
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|a EC 3.4.22.-
|2 NLM
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|a Calpain
|2 NLM
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| 650 |
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|a EC 3.4.22.-
|2 NLM
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| 700 |
1 |
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|a Yu, Shengxue
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Zhao, Fang
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Liu, Yu
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Wang, Yue
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Fan, Siqi
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Su, Yuhong
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Lu, Meili
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Wang, Hongxin
|e verfasserin
|4 aut
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| 773 |
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|i Enthalten in
|t Neural plasticity
|d 1998
|g 2022(2022) vom: 20., Seite 6509981
|w (DE-627)NLM098558390
|x 1687-5443
|7 nnas
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| 773 |
1 |
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|g volume:2022
|g year:2022
|g day:20
|g pages:6509981
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|u http://dx.doi.org/10.1155/2022/6509981
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