• Dongdong Sun, Jianhao Wang, Xilei Liu, Yueshan Fan, Mengchen Yang, and Jianning Zhang.
• Department of Neurosurgery, Tianjin Medical University General Hospital, 154 Anshan Road, Tianjin 300052, China; Tianjin Neurological Institute, Key Laboratory of Post-Neuroinjury Neuro-Repair and Regeneration in Central Nervous System, Ministry of Education and Tianjin City, 154 Anshan Road, Tianjin 300052, China. Electronic address: sundongdong0210@163.com.
• Brain Res. 2020 Apr 1; 1732: 146682.

AbstractTraumatic brain injury (TBI) is one of the leading causes of mortality and disability worldwide. Emerging studies have shown that endoplasmic reticulum (ER) stress plays an important role in the pathophysiology of TBI. Dexmedetomidine (Dex), a highly selective α2-adrenoreceptor agonist, has been shown to attenuate ER stress. However, there is no relevant research in the field of TBI. To study the effects of dexmedetomidine on TBI, we subjected mice to TBI with a controlled cortical impact (CCI) device. The expression levels of ER stress marker proteins and apoptosis-related proteins were evaluated by western blotting and immunofluorescence. Neuronal cell death was assessed by a terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick end-labelling (TUNEL) assay. Neurological and motor deficits were assessed by modified neurological severity scores (mNSSs) and beam balance and beam walking tests. Brain water content and EB leakage were also assessed. Our group found that ER stress was significantly activated 72 h after TBI. Dexmedetomidine significantly reduced ER stress and ER stress-related neuronal apoptosis induced by experimental TBI. In addition, dexmedetomidine significantly improved neurological function and alleviated brain oedema. These findings indicate that dexmedetomidine alleviates severe, post-traumatic ER stress and attenuates secondary brain damage.Copyright © 2020 Elsevier B.V. All rights reserved.

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