Protein profiling identified mitochondrial dysfunction and synaptic abnormalities after dexamethasone intervention in rats with traumatic brain injury
Protein profiling identified mitochondrial dysfunction and synaptic abnormalities after dexamethasone intervention in rats with traumatic brain injury作者机构:Department of NeurotraumaBeijing Key Laboratory of Central Nervous System InjuryBeijing Neurosurgical InstituteCapital Medical UniversityBeijingChina Department of NeurosurgeryBeijing Tiantan HospitalCapital Medical UniversityBeijingChina Key Laboratory of Central Nervous System Injury ResearchCenter for Brain TumorBeijing Institute of Brain DisordersBeijing Neurosurgical InstituteCapital Medical UniversityBeijingChina Department of Neurosurgerythe First Affiliated Hospital of Anhui Medical UniversityHefeiAnhui ProvinceChina Center for Nerve Injury and RepairBeijing Institute of Brain DisordersBeijingChina China National Clinical Research Center for Neurological DiseasesBeijingChina
出 版 物:《Neural Regeneration Research》 (中国神经再生研究(英文版))
年 卷 期:2021年第16卷第12期
页 面:2438-2445页
核心收录:
学科分类:1002[医学-临床医学] 1010[医学-医学技术(可授医学、理学学位)] 100215[医学-康复医学与理疗学] 100204[医学-神经病学] 10[医学]
基 金:This study was supported by the National Natural Science Foundation of China,No.81771327(to BYL) the Platform Construction of Basic Research and Clinical Translation of Nervous System Injury,China,No.PXM2020_026280_000002(to BYL) the Scientific Research and Cultivation Fund of the Beijing Neurosurgical Institute,China,No.2020002(to FN)
主 题:dexamethasone Gria3 Maob mass spectrometry mitochondrial dysfunction Ndufs2 Ndufv2 proteomics synaptic abnormalities traumatic brain injury
摘 要:Dexamethasone has been widely used after various neurosurgical procedures due to its anti-inflammatory property and the abilities to restore vascular permeability,inhibit free radicals,and reduce cerebrospinal fluid *** to the latest guidelines for the treatment of traumatic brain injury in the United States,high-dose glucocorticoids cause neurological *** investigate the reason why high-dose glucocorticoids after traumatic brain injury exhibit harmful effect,rat controlled cortical impact models of traumatic brain injury were *** 1 hour and 2 days after surgery,rat models were intraperitoneally administered dexamethasone 10 mg/*** results revealed that 31 proteins were significantly upregulated and 12 proteins were significantly downregulated in rat models of traumatic brain injury after dexamethasone *** Ingenuity Pathway Analysis results showed that differentially expressed proteins were enriched in the mitochondrial dysfunction pathway and synaptogenesis signaling *** blot analysis and immunohistochemistry results showed that Ndufv2,Maob and Gria3 expression and positive cell count in the dexamethasone-treated group were significantly greater than those in the model *** findings suggest that dexamethasone may promote a compensatory increase in complex I subunits(Ndufs2 and Ndufv2),increase the expression of mitochondrial enzyme Maob,and upregulate synaptic-transmission-related protein *** changes may be caused by nerve injury after traumatic brain injury treatment by *** study was approved by Institutional Ethics Committee of Beijing Neurosurgical Institute(approval No.201802001)on June 6,2018.