Controlled Decompression Attenuates Compressive Injury following Traumatic Brain Injury via TREK-1-Mediated Inhibition of Necroptosis and Neuroinflammation

Decompressive craniectomy is an effective strategy to reduce intracranial hypertension after traumatic brain injury (TBI), but it is related to many postoperative complications, such as delayed intracranial hematoma and diffuse brain swelling. Our previous studies have demonstrated that controlled d...

Descripción completa

Guardado en:

Detalles Bibliográficos
Autores principales:	Tao Chen, Xiao Qian, Jie Zhu, Li-Kun Yang, Yu-Hai Wang
Formato:	article
Lenguaje:	EN
Publicado:	Hindawi Limited 2021
Materias:	Cytology QH573-671
Acceso en línea:	https://doaj.org/article/869c65b504e047e58924c8368dc127c1
Etiquetas:	Agregar Etiqueta Sin Etiquetas, Sea el primero en etiquetar este registro!

id	oai:doaj.org-article:869c65b504e047e58924c8368dc127c1
record_format	dspace
spelling	oai:doaj.org-article:869c65b504e047e58924c8368dc127c12021-11-22T01:09:50ZControlled Decompression Attenuates Compressive Injury following Traumatic Brain Injury via TREK-1-Mediated Inhibition of Necroptosis and Neuroinflammation1942-099410.1155/2021/4280951https://doaj.org/article/869c65b504e047e58924c8368dc127c12021-01-01T00:00:00Zhttp://dx.doi.org/10.1155/2021/4280951https://doaj.org/toc/1942-0994Decompressive craniectomy is an effective strategy to reduce intracranial hypertension after traumatic brain injury (TBI), but it is related to many postoperative complications, such as delayed intracranial hematoma and diffuse brain swelling. Our previous studies have demonstrated that controlled decompression (CDC) surgery attenuates brain injury and reduces the rate of complications after TBI. Here, we investigated the potential molecular mechanisms of CDC in experimental models. The in vitro experiments were performed in a traumatic neuronal injury (TNI) model following compression treatment in primary cultured cortical neurons. We found that compression aggravates TNI-induced neuronal injury, which was significantly attenuated by CDC for 2 h or 3 h. The results of immunocytochemistry showed that CDC reduced neuronal necroptosis and activation of RIP3 induced by TNI and compression, with no effect on RIP1 activity. These protective effects were associated with decreased levels of inflammatory cytokines and preserved intracellular Ca2+ homeostasis. In addition, the expression of the two-pore domain K+ channel TREK-1 and its activity was increased by compression and prolonged by CDC. Treatment with the TREK-1 blockers, spadin or SID1900, could partially prevent the effects of CDC on intracellular Ca2+ metabolism, necroptosis, and neuronal injury following TNI and compression. Using a traumatic intracranial hypertension model in rats, we found that CDC for 20 min or 30 min was effective in alleviating brain edema and locomotor impairment in vivo. CDC significantly inhibited neuronal necroptosis and neuroinflammation and increased TREK-1 activation, and the CDC-induced protection in vivo was attenuated by spadin and SID1900. In summary, CDC is effective in alleviating compressive neuronal injury both in vitro and in vivo, which is associated with the TREK-1-mediated attenuation of intracellular Ca2+ overload, neuronal necroptosis, and neuroinflammation.Tao ChenXiao QianJie ZhuLi-Kun YangYu-Hai WangHindawi LimitedarticleCytologyQH573-671ENOxidative Medicine and Cellular Longevity, Vol 2021 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Cytology QH573-671
spellingShingle	Cytology QH573-671 Tao Chen Xiao Qian Jie Zhu Li-Kun Yang Yu-Hai Wang Controlled Decompression Attenuates Compressive Injury following Traumatic Brain Injury via TREK-1-Mediated Inhibition of Necroptosis and Neuroinflammation
description	Decompressive craniectomy is an effective strategy to reduce intracranial hypertension after traumatic brain injury (TBI), but it is related to many postoperative complications, such as delayed intracranial hematoma and diffuse brain swelling. Our previous studies have demonstrated that controlled decompression (CDC) surgery attenuates brain injury and reduces the rate of complications after TBI. Here, we investigated the potential molecular mechanisms of CDC in experimental models. The in vitro experiments were performed in a traumatic neuronal injury (TNI) model following compression treatment in primary cultured cortical neurons. We found that compression aggravates TNI-induced neuronal injury, which was significantly attenuated by CDC for 2 h or 3 h. The results of immunocytochemistry showed that CDC reduced neuronal necroptosis and activation of RIP3 induced by TNI and compression, with no effect on RIP1 activity. These protective effects were associated with decreased levels of inflammatory cytokines and preserved intracellular Ca2+ homeostasis. In addition, the expression of the two-pore domain K+ channel TREK-1 and its activity was increased by compression and prolonged by CDC. Treatment with the TREK-1 blockers, spadin or SID1900, could partially prevent the effects of CDC on intracellular Ca2+ metabolism, necroptosis, and neuronal injury following TNI and compression. Using a traumatic intracranial hypertension model in rats, we found that CDC for 20 min or 30 min was effective in alleviating brain edema and locomotor impairment in vivo. CDC significantly inhibited neuronal necroptosis and neuroinflammation and increased TREK-1 activation, and the CDC-induced protection in vivo was attenuated by spadin and SID1900. In summary, CDC is effective in alleviating compressive neuronal injury both in vitro and in vivo, which is associated with the TREK-1-mediated attenuation of intracellular Ca2+ overload, neuronal necroptosis, and neuroinflammation.
format	article
author	Tao Chen Xiao Qian Jie Zhu Li-Kun Yang Yu-Hai Wang
author_facet	Tao Chen Xiao Qian Jie Zhu Li-Kun Yang Yu-Hai Wang
author_sort	Tao Chen
title	Controlled Decompression Attenuates Compressive Injury following Traumatic Brain Injury via TREK-1-Mediated Inhibition of Necroptosis and Neuroinflammation
title_short	Controlled Decompression Attenuates Compressive Injury following Traumatic Brain Injury via TREK-1-Mediated Inhibition of Necroptosis and Neuroinflammation
title_full	Controlled Decompression Attenuates Compressive Injury following Traumatic Brain Injury via TREK-1-Mediated Inhibition of Necroptosis and Neuroinflammation
title_fullStr	Controlled Decompression Attenuates Compressive Injury following Traumatic Brain Injury via TREK-1-Mediated Inhibition of Necroptosis and Neuroinflammation
title_full_unstemmed	Controlled Decompression Attenuates Compressive Injury following Traumatic Brain Injury via TREK-1-Mediated Inhibition of Necroptosis and Neuroinflammation
title_sort	controlled decompression attenuates compressive injury following traumatic brain injury via trek-1-mediated inhibition of necroptosis and neuroinflammation
publisher	Hindawi Limited
publishDate	2021
url	https://doaj.org/article/869c65b504e047e58924c8368dc127c1
work_keys_str_mv	AT taochen controlleddecompressionattenuatescompressiveinjuryfollowingtraumaticbraininjuryviatrek1mediatedinhibitionofnecroptosisandneuroinflammation AT xiaoqian controlleddecompressionattenuatescompressiveinjuryfollowingtraumaticbraininjuryviatrek1mediatedinhibitionofnecroptosisandneuroinflammation AT jiezhu controlleddecompressionattenuatescompressiveinjuryfollowingtraumaticbraininjuryviatrek1mediatedinhibitionofnecroptosisandneuroinflammation AT likunyang controlleddecompressionattenuatescompressiveinjuryfollowingtraumaticbraininjuryviatrek1mediatedinhibitionofnecroptosisandneuroinflammation AT yuhaiwang controlleddecompressionattenuatescompressiveinjuryfollowingtraumaticbraininjuryviatrek1mediatedinhibitionofnecroptosisandneuroinflammation
_version_	1718418410765811712

Controlled Decompression Attenuates Compressive Injury following Traumatic Brain Injury via TREK-1-Mediated Inhibition of Necroptosis and Neuroinflammation

Ejemplares similares