The effect of high mobility group box-1 protein on cerebral edema, blood-brain barrier, oxidative stress and apoptosis in an experimental traumatic brain injury model

Autor: Abdurrahim Kocyigit, Salim Katar, Mustafa Aziz Hatiboglu, Enes Akkaya, Ersin Karataş, Ebru Gürel Gürevin, Hakan Hanimoglu, Oguz Baran, Fatih Çalış, Elif Ilkay Armutak, Serdar Cevik, Sevket Evran, Mehmet Yasar Kaynar
Přispěvatelé: HATİBOĞLU, MUSTAFA AZİZ
Rok vydání: 2020
Předmět:
Male
0301 basic medicine
medicine.medical_specialty
Traumatic brain injury
Receptor for Advanced Glycation End Products
Apoptosis
Brain Edema
Blood–brain barrier
medicine.disease_cause
Occludin
HMGB1
Cerebral edema
Rats
Sprague-Dawley
03 medical and health sciences
0302 clinical medicine
Internal medicine
Brain Injuries
Traumatic
medicine
Animals
Claudin-5
HMGB1 Protein
Pyruvates
Neuroinflammation
biology
business.industry
General Neuroscience
High Mobility Group Proteins
Evran S.
Calis F.
Akkaya E.
Baran O.
Cevik S.
Katar S.
Gurevin E. G.
Hanimoglu H.
Hatiboglu M. A.
Armutak E. I.
et al.
-The effect of high mobility group box-1 protein on cerebral edema
blood-brain barrier
oxidative stress and apoptosis in an experimental traumatic brain injury model-
Brain Research Bulletin
cilt.154
ss.68-80
2020
Brain
medicine.disease
Pathophysiology
Rats
Toll-Like Receptor 4
Disease Models
Animal
Oxidative Stress
030104 developmental biology
medicine.anatomical_structure
Endocrinology
Blood-Brain Barrier
Brain Injuries
HMG-Box Domains
Zonula Occludens-1 Protein
biology.protein
business
030217 neurology & neurosurgery
Oxidative stress
Zdroj: Brain Research Bulletin. 154:68-80
ISSN: 0361-9230
DOI: 10.1016/j.brainresbull.2019.10.013
Popis: Traumatic brain injury (TBI) is one of the important reason of morbidity and mortality. While the primary injury due to mechanical impact is unavoidable, the secondary injury which is formed as a result of primary injury and thought to occur due to neuroinflammation in the forefront can be prevented and by this way mortality and morbidity can be reduced. High mobility group box-1 (HMGB1) is a protein that triggers the neuroinflammatory process by being released from the nucleus of necrotic tissues after primary injury. The aim of this study is to investigate the effects of HMGB1 on its receptors TLR4 and RAGE, cerebral edema, blood-brain barrier, oxidative stress and apoptosis causing secondary damage in an experimental traumatic brain injury model. Weighing between 280–320 g, 10 to 12 weeks-old, a total of 30 adult male Sprague-Dawley rats were used for the experiments. The rats were randomly assigned to 3 groups: 1) Control, 2) TBI and 3) TBI + ethyl pyruvate group (n = 10 per group). Right parietal cortical contusion was made by using a weight-dropping TBI method. Brain samples were harvested from pericontusional area at 24 h after TBI. HMGB1, TLR4, RAGE, occludin, claudin-5, ZO-1 levels are investigated by western blot analyses and immunohistochemistry examinations. HMGB-1, TLR4 and RAGE expressions increased after TBI. Major tight junction proteins in the blood-brain barrier: occludin, claudin-5 and ZO-1 expressions decreased after TBI. Brain edema increased after TBI. Also, proapoptotic bax and active caspase 3 expressions increased, antiapoptotic bcl-2 levels decreased after TBI. Total oxidant status and oxidative stress increased, total antioxidant status decreased after TBI. HMGB-1 protein plays a key role in the pathophysiology of traumatic brain injury.
Databáze: OpenAIRE
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