Effectiveness of gfap in determining neuron damage in rats with induced head trauma

Abstract

spread neurodegeneration and is still a major worldwide health problem (2,33,44,50,51). TBI causes not only direct mechanical damage to the brain, but it also induces biochemical changes that lead to delayed neural cell loss. These biochemical changes are called secondary injury. The primary █ INTRODUCTION O ne common form of acute brain injury, traumatic brain injury (TBI), is the result of an outside force causing immediate mechanical disruption of brain tissue and delayed pathogenic events that collectively mediate wideAIm: To determine whether the serum level of glial fibrillary acidic protein (GFAP), an important indicator of neuron damage, correlates with the extent of tissue damage in the rat with induced head trauma and to obtain data in order to avoid unnecessary cranial computed tomography analyses. mATERIAl and mEThODS: Three-month-old male Sprague-Dawley rats were used. Rats were divided into 5 groups. The experimental head trauma model was examined in five groups (n=8) as follows: The control group had no intervention; Group 1: Head trauma was induced by dropping a 25 mg ball from a height of 20 cm; Group 2: Head trauma was induced by dropping a 50 mg ball from a height of 20 cm; Group 3: Head trauma was induced by dropping a 50 mg ball from a height of 80 cm; Group 4: Head trauma was induced by dropping a 100 mg ball from a height of 80 cm. Thus, according to the Newton's Law, respectively 0.05, 0.1, 0.2 and 0.4 N trauma was created. Serum GFAP levels were analyzed and the damage to cerebral tissues was evaluated in all groups. RESUlTS:We determined that number of apoptotic cells and particularly the number of GFAP (+) protoplasmic astrocytes at the perilesional region of the cortex increased in association with the increased serum GFAP level as long as the severity of the trauma increased.CONClUSION: Serum GFAP concentration can be used as a marker of the severity of head trauma and traumatic brain injury. However, more animal studies are required to reflect this result in clinical practice.

Sitagliptin Attenuates the Cognitive Deficits in L-Methionine-Induced Vascular Dementia in Rats

“…Baydas et al [ 68 ] attributed that to HHcy-induced glial cell sensitization. Moreover, previous studies clarified that increased tissue GFAP immunoreactivity was a sensitive indicator of neuronal injury and neuroinflammation [ 69 , 70 ]. However, the VaD + STG group results revealed significant downregulation of GFAP immunoreaction when compared with the VaD group.…”

Ubiquinol treatment for TBI in male rats: Effects on mitochondrial integrity, injury severity, and neurometabolism

“…* Significantly different from Saline-TBI [Color figure can be viewed at wileyonlinelibrary.com] identifying successful therapeutic approaches to reduce TBI secondary injury (Di Battista et al, 2015). GFAP is an intermediate filament protein specific for astrocytes, and increased GFAP immunoreactivity is a sensitive astrocyte injury biomarker (Cikriklar et al, 2016;Lei et al, 2015;Mondello et al, 2016). GFAP protein is rapidly released into biofluids following cortical injury (Foerch et al, 2012;Y.…”

Cortical Electrical Stimulation Ameliorates Traumatic Brain Injury-Induced Sensorimotor and Cognitive Deficits in Rats

“…GFAP is an astrocyte-specific intermediate filament component of the central nervous system (CNS) and is a common target used for observing the astroglial responses after TBI in vivo experiments (Myer et al, 2006 ; Chen et al, 2012 ). The astrocytes respond to TBI by pronounced changes in cell proliferation and cellular hypertrophy in the lesion site (Myer et al, 2006 ; Babaee et al, 2015 ; Cikriklar et al, 2016 ). In our earlier study using the same diffuse TBI rat model, the upregulation of GFAP has been found at day 1 and remained elevated for at least 1-week post TBI-lesion (Hsieh et al, 2017 ).…”