Immunological Response in Early Brain Injury After SAH

2011 ◽  
pp. 57-61 ◽  
Author(s):  
Takumi Sozen ◽  
Reiko Tsuchiyama ◽  
Yu Hasegawa ◽  
Hidenori Suzuki ◽  
Vikram Jadhav ◽  
...  
Keyword(s):  
Brain Injury ◽  
Immunological Response ◽  
Early Brain Injury

scholarly journals TRAF3 mediates neuronal apoptosis in early brain injury following subarachnoid hemorrhage via targeting TAK1-dependent MAPKs and NF-κB pathways

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Yan Zhou ◽  
Tao Tao ◽  
Guangjie Liu ◽  
Xuan Gao ◽  
Yongyue Gao ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Brain Injury ◽  
Therapeutic Target ◽  
Cortical Neurons ◽  
Neuronal Apoptosis ◽  
Early Brain Injury ◽  
Neurological Deficits ◽  
Human Brain Tissue

AbstractNeuronal apoptosis has an important role in early brain injury (EBI) following subarachnoid hemorrhage (SAH). TRAF3 was reported as a promising therapeutic target for stroke management, which covered several neuronal apoptosis signaling cascades. Hence, the present study is aimed to determine whether downregulation of TRAF3 could be neuroprotective in SAH-induced EBI. An in vivo SAH model in mice was established by endovascular perforation. Meanwhile, primary cultured cortical neurons of mice treated with oxygen hemoglobin were applied to mimic SAH in vitro. Our results demonstrated that TRAF3 protein expression increased and expressed in neurons both in vivo and in vitro SAH models. TRAF3 siRNA reversed neuronal loss and improved neurological deficits in SAH mice, and reduced cell death in SAH primary neurons. Mechanistically, we found that TRAF3 directly binds to TAK1 and potentiates phosphorylation and activation of TAK1, which further enhances the activation of NF-κB and MAPKs pathways to induce neuronal apoptosis. Importantly, TRAF3 expression was elevated following SAH in human brain tissue and was mainly expressed in neurons. Taken together, our study demonstrates that TRAF3 is an upstream regulator of MAPKs and NF-κB pathways in SAH-induced EBI via its interaction with and activation of TAK1. Furthermore, the TRAF3 may serve as a novel therapeutic target in SAH-induced EBI.

Clarithromycin Ameliorates Early Brain Injury After Subarachnoid Hemorrhage via Suppressing Periostin-Related Pathways in Mice

2021 ◽  
Author(s):  
Hideki Kanamaru ◽  
Fumihiro Kawakita ◽  
Hirofumi Nishikawa ◽  
Fumi Nakano ◽  
Reona Asada ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Brain Injury ◽  
Early Brain Injury

scholarly journals Biglycan regulates neuroinflammation by promoting M1 microglial activation in early brain injury after experimental subarachnoid hemorrhage

2019 ◽  
Vol 152 (3) ◽  
pp. 368-380 ◽  
Author(s):  
Yuke Xie ◽  
Jianhua Peng ◽  
Jinwei Pang ◽  
Kecheng Guo ◽  
Lifang Zhang ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Brain Injury ◽  
Microglial Activation ◽  
Early Brain Injury ◽  
Experimental Subarachnoid Hemorrhage

scholarly journals Expression signatures of long non-coding RNAs in early brain injury following experimental subarachnoid hemorrhage

2015 ◽  
Vol 12 (1) ◽  
pp. 967-973 ◽  
Author(s):  
BINGJIE ZHENG ◽  
HUAILEI LIU ◽  
RUKE WANG ◽  
SHANCAI XU ◽  
YAOHUA LIU ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Brain Injury ◽  
Early Brain Injury ◽  
Experimental Subarachnoid Hemorrhage ◽  
Non Coding Rnas

Treatment of early brain injury after subarachnoid hemorrhage in the rat model by inhibiting p53-induced ferroptosis

2021 ◽  
pp. 136134
Author(s):  
Hong Kuang ◽  
Tianhong Wang ◽  
Lei Liu ◽  
Chunhai Tang ◽  
Tao Li ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Brain Injury ◽  
Rat Model ◽  
Early Brain Injury

Apigenin attenuates oxidative stress and neuronal apoptosis in early brain injury following subarachnoid hemorrhage

2017 ◽  
Vol 40 ◽  
pp. 157-162 ◽  
Author(s):  
Yuwei Han ◽  
Tingting Zhang ◽  
Jingyuan Su ◽  
Yuan Zhao ◽  
Chenchen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Subarachnoid Hemorrhage ◽  
Brain Injury ◽  
Neuronal Apoptosis ◽  
Early Brain Injury
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