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Tytuł:
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Taraxasterol protects hippocampal neurons from oxygen-glucose deprivation-induced injury through activation of Nrf2 signalling pathway.
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Autorzy:
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He Y; Department of Neurology, AnKang Central Hospital, AnKang, China.
Jiang K; Department of Neurology, AnKang Central Hospital, AnKang, China.
Zhao X; Department of Neurology, AnKang Central Hospital, AnKang, China.
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Źródło:
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Artificial cells, nanomedicine, and biotechnology [Artif Cells Nanomed Biotechnol] 2020 Dec; Vol. 48 (1), pp. 252-258.
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Typ publikacji:
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Journal Article
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Język:
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English
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Imprint Name(s):
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Publication: 2015- : Abingdon, Oxford : Taylor & Francis
Original Publication: London : Informa Healthcare, [2013]-
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MeSH Terms:
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Glucose/*deficiency
Hippocampus/*cytology
NF-E2-Related Factor 2/*metabolism
Neurons/*drug effects
Oxygen/*metabolism
Signal Transduction/*drug effects
Sterols/*pharmacology
Triterpenes/*pharmacology
Animals ; Apoptosis/drug effects ; Cytoprotection/drug effects ; Female ; Mice ; Neurons/cytology ; Neurons/metabolism ; Oxidative Stress/drug effects ; Pregnancy
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Contributed Indexing:
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Keywords: Ischaemic stroke; Nrf2 signalling pathway; cell apoptosis; cerebral ischemia/reperfusion (I/R) injury; oxidative stress; taraxasterol
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Substance Nomenclature:
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0 (NF-E2-Related Factor 2)
0 (Nfe2l2 protein, mouse)
0 (Sterols)
0 (Triterpenes)
64SK2ERN9P (taraxasterol)
IY9XDZ35W2 (Glucose)
S88TT14065 (Oxygen)
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Entry Date(s):
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Date Created: 20191219 Date Completed: 20200601 Latest Revision: 20200601
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Update Code:
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20240105
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DOI:
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10.1080/21691401.2019.1699831
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PMID:
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31851841
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Cerebral ischemia/reperfusion (I/R) injury is a brain injury following ischaemic stroke that is associated with oxidative stress. Taraxasterol, a natural product, has been shown to have anti-oxidative and neuro-protective effects. However, the role of taraxasterol in cerebral I/R injury remains unknown. Primary hippocampal neurons were subjected to oxygen-glucose deprivation/reperfusion (OGD/R) to induce cerebral I/R injury in vitro . Cell viability of hippocampal neurons was measured CCK-8 assay. Reactive oxygen species (ROS) production and MDA generation were measured to reflect oxidative stress. Western blotting was performed to evaluate the expressions of bax, bcl-2, NF-E2-related factor 2 (Nrf2), haem oxygenase (HO-1), NAD(P)H:quinone oxidoreductase 1 (NQO-1) and GPx-3. Caspase-3 activity was measured to assess cell apoptosis. Hippocampal neurons were treated with ML385 to inhibit Nrf2 signalling pathway. Our results showed that taraxasterol improved OGD/R-caused decrease in cell viability of hippocampal neurons. In addition, taraxasterol significantly suppressed ROS production and MDA generation in OGD/R-induced hippocampal neurons. Taraxasterol resulted in a significant decrease in caspase-3 activity and bcl-2 expression, as well as increase in bax expression. Furthermore, taraxasterol induced the Nrf2 nuclear accumulation and expressions of HO-1, NQO-1 and GPx-3 in OGD/R-induced hippocampal neurons. Notably, inhibition of Nrf2 signalling reversed the protective effects of taraxasterol on OGD/R-induced hippocampal neurons injury. In conclusion, these findings indicated that taraxasterol protected hippocampal neurons from OGD/R-induced oxidative stress and cell apoptosis via regulating the Nrf2 signalling pathway.
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