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Tetrandrine alleviates inflammation and neuron apoptosis in experimental traumatic brain injury by regulating the IRE1α/JNK/CHOP signal pathway

AIM: The aim of this study was to investigate the therapeutic roles of Tetrandrine (TET) on traumatic brain injury (TBI) and the underlying mechanism. METHOD: Traumatic injury model of hippocampal neurons and TBI mouse model were established to evaluate the therapeutic effects. The expression of neu...

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Autores principales: Liu, Huan, He, Shiqing, Li, Chong, Wang, Jianpeng, Zou, Qin, Liao, Yongshi, Chen, Rui
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9759135/
https://www.ncbi.nlm.nih.gov/pubmed/36377337
http://dx.doi.org/10.1002/brb3.2786
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author Liu, Huan
He, Shiqing
Li, Chong
Wang, Jianpeng
Zou, Qin
Liao, Yongshi
Chen, Rui
author_facet Liu, Huan
He, Shiqing
Li, Chong
Wang, Jianpeng
Zou, Qin
Liao, Yongshi
Chen, Rui
author_sort Liu, Huan
collection PubMed
description AIM: The aim of this study was to investigate the therapeutic roles of Tetrandrine (TET) on traumatic brain injury (TBI) and the underlying mechanism. METHOD: Traumatic injury model of hippocampal neurons and TBI mouse model were established to evaluate the therapeutic effects. The expression of neuron‐specific enolase (NSE), Caspase 3, and Caspase 12 was detected by immunofluorescence. The expression of TNF‐α, NF‐κB, TRAF1, ERS markers (GADD34 and p‐PERK), IRE1α, CHOP, JNK, and p‐JNK were evaluated by western blot. Flow cytometry was used to determine the apoptosis of neurons. Brain injury was assessed by Garcia score, cerebral water content, and Evan blue extravasation test. Hematoxylin and eosin staining was used to determine the morphological changes of hippocampal tissue. Apoptosis was assessed by TUNEL staining. RESULT: In traumatic injury model of hippocampal neurons, TET downregulated NSE, TNF‐α, NF‐κB, TRAF1, GADD34, p‐PERK, IRE1α, CHOP, and p‐JNK expression. TET reduced Caspase 3 and Caspase 12 cleavage. Apoptosis rate was inhibited by the introduction of TET. TET improved the Garcia neural score, decreased the cerebral water content and Evans blue extravasation, and reduced NSE, TNF‐α, NF‐κB, TRAF1, IRE1α, CHOP, and p‐JNK expression in mice with TBI, which was significantly reversed by Anisomycin, a JNK selective activator. CONCLUSION: TET alleviated inflammation and neuron apoptosis in experimental TBI by regulating the IRE1α/JNK/CHOP signal pathway.
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spelling pubmed-97591352022-12-20 Tetrandrine alleviates inflammation and neuron apoptosis in experimental traumatic brain injury by regulating the IRE1α/JNK/CHOP signal pathway Liu, Huan He, Shiqing Li, Chong Wang, Jianpeng Zou, Qin Liao, Yongshi Chen, Rui Brain Behav Original Articles AIM: The aim of this study was to investigate the therapeutic roles of Tetrandrine (TET) on traumatic brain injury (TBI) and the underlying mechanism. METHOD: Traumatic injury model of hippocampal neurons and TBI mouse model were established to evaluate the therapeutic effects. The expression of neuron‐specific enolase (NSE), Caspase 3, and Caspase 12 was detected by immunofluorescence. The expression of TNF‐α, NF‐κB, TRAF1, ERS markers (GADD34 and p‐PERK), IRE1α, CHOP, JNK, and p‐JNK were evaluated by western blot. Flow cytometry was used to determine the apoptosis of neurons. Brain injury was assessed by Garcia score, cerebral water content, and Evan blue extravasation test. Hematoxylin and eosin staining was used to determine the morphological changes of hippocampal tissue. Apoptosis was assessed by TUNEL staining. RESULT: In traumatic injury model of hippocampal neurons, TET downregulated NSE, TNF‐α, NF‐κB, TRAF1, GADD34, p‐PERK, IRE1α, CHOP, and p‐JNK expression. TET reduced Caspase 3 and Caspase 12 cleavage. Apoptosis rate was inhibited by the introduction of TET. TET improved the Garcia neural score, decreased the cerebral water content and Evans blue extravasation, and reduced NSE, TNF‐α, NF‐κB, TRAF1, IRE1α, CHOP, and p‐JNK expression in mice with TBI, which was significantly reversed by Anisomycin, a JNK selective activator. CONCLUSION: TET alleviated inflammation and neuron apoptosis in experimental TBI by regulating the IRE1α/JNK/CHOP signal pathway. John Wiley and Sons Inc. 2022-11-14 /pmc/articles/PMC9759135/ /pubmed/36377337 http://dx.doi.org/10.1002/brb3.2786 Text en © 2022 The Authors. Brain and Behavior published by Wiley Periodicals LLC. https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Articles
Liu, Huan
He, Shiqing
Li, Chong
Wang, Jianpeng
Zou, Qin
Liao, Yongshi
Chen, Rui
Tetrandrine alleviates inflammation and neuron apoptosis in experimental traumatic brain injury by regulating the IRE1α/JNK/CHOP signal pathway
title Tetrandrine alleviates inflammation and neuron apoptosis in experimental traumatic brain injury by regulating the IRE1α/JNK/CHOP signal pathway
title_full Tetrandrine alleviates inflammation and neuron apoptosis in experimental traumatic brain injury by regulating the IRE1α/JNK/CHOP signal pathway
title_fullStr Tetrandrine alleviates inflammation and neuron apoptosis in experimental traumatic brain injury by regulating the IRE1α/JNK/CHOP signal pathway
title_full_unstemmed Tetrandrine alleviates inflammation and neuron apoptosis in experimental traumatic brain injury by regulating the IRE1α/JNK/CHOP signal pathway
title_short Tetrandrine alleviates inflammation and neuron apoptosis in experimental traumatic brain injury by regulating the IRE1α/JNK/CHOP signal pathway
title_sort tetrandrine alleviates inflammation and neuron apoptosis in experimental traumatic brain injury by regulating the ire1α/jnk/chop signal pathway
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9759135/
https://www.ncbi.nlm.nih.gov/pubmed/36377337
http://dx.doi.org/10.1002/brb3.2786
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