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Expression of VEGF and GFAP in a rat model of traumatic brain injury treated with Honokiol: a biochemical and immunohistochemical study
Expression of VEGF and GFAP in a rat model of traumatic brain injury treated with Honokiol: a biochemical and immunohistochemical study
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Expression of VEGF and GFAP in a rat model of traumatic brain injury treated with Honokiol: a biochemical and immunohistochemical study
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Expression of VEGF and GFAP in a rat model of traumatic brain injury treated with Honokiol: a biochemical and immunohistochemical study
Expression of VEGF and GFAP in a rat model of traumatic brain injury treated with Honokiol: a biochemical and immunohistochemical study

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Expression of VEGF and GFAP in a rat model of traumatic brain injury treated with Honokiol: a biochemical and immunohistochemical study
Expression of VEGF and GFAP in a rat model of traumatic brain injury treated with Honokiol: a biochemical and immunohistochemical study
Journal Article

Expression of VEGF and GFAP in a rat model of traumatic brain injury treated with Honokiol: a biochemical and immunohistochemical study

2019
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Overview
Traumatic brain injury leads to neuronal damage and neurological dysfunction. The aim of our study was to investigate the antioxidative effect of Honokiol on traumatic brain injury in rats with biochemical, histopathological and immunohistochemical methods. Sprague-Dawley rats were subjected to traumatic brain injury with a weight-drop device using 300g/1m weight/height impact. Fourty five rats were divided into three groups as control group, traumatic brain injury (TBI) group and TBI + Honokiol group (5 mg/kg/day, i.p.). Honokiol (5 mg/kg) dissolved in dimethyl sulfoxide (DMSO) was intraperitoneally administered to rats for 7 days after the trauma. At the end of experiment, blood samples were taken from the animals and analyzed with various biochemical markers. Histopathological examination of the trauma group revealed some degenerated pyramidal cells, dilatation and congestion in blood vessels, hyperplasia in endothelial cells, inflammatory cell infiltration around the vein and disruptions in glial extensions. In TBI + Honokiol group, pyramidal neurons showed a decrease in degeneration, slight dilatation in blood vessels, improvement of endothelial cells towards the lumen, and reduction of inflammatory cells in the vessel. In TBI + Honokiol group, vascular endothelial growth factor (VEGF) expression was positive in the endothelial and few inflammatory cells of the mildly dilated blood vessels. In the blood brain barrier deteriorated after trauma, it was observed that the glial foot processes were positive expression and extended to the endothelial cells in the TBI + Honokiol group. Glial fibrillary acidic protein (GFAP) expression showed a positive reaction in these processes. Considering the important role of antioxidants and inflammatory responses in cerebral damage induced by traumatic head injury, honokiol is thought to be important in decreasing lipid peroxidation, protecting the membrane structure of blood brain barrier, degeneration of neurons and glial cells.

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