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- 저자 : Deveci Engin (검색결과 2 건)
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Ganoderma Lucidum Protects Rat Brain Tissue Against Trauma-Induced Oxidative Stress
Özevren Hüseyin,İrtegün Sevgi,Deveci Engin,Aşır Fırat,Pektanç Gülsüm,Deveci Şenay 대한신경손상학회 2017 Korean Journal of Neurotrauma Vol.14 No.2
Objective: Traumatic brain injury causes tissue damage, breakdown of cerebral blood flow and metabolic regulation. Thisstudy aims to investigate the protective influence of antioxidant Ganoderma lucidum (G. lucidum) polysaccharides (GLPs)on brain injury in brain-traumatized rats. Methods: Sprague-Dawley conducted a head-traumatized method on rats by dropping off 300 g weight from 1 m height. Groups were categorized as control, G. lucidum, trauma, trauma+ G. lucidum (20 mL/kg per day via gastric gavage). Braintissues were dissected from anesthetized rats 7 days after injury. For biochemical analysis, malondialdehyde, glutathioneand myeloperoxidase values were measured. Results: In histopathological examination, neuronal damage in brain cortex and changes in blood brain barrier were observed. In the analysis of immunohistochemical and western blot, p38 mitogen-activated protein kinase, vascular endothelial growth factor and cluster of differentiation 68 expression levels were shown. These analyzes demonstrated the benefcial effects of GLPs on brain injury. Conclusion: We propose that GLPs treatment after brain injury could be an alternative treatment to decraseing inflammationand edema, preventing neuronal and glial cells degeneration if given in appropriate dosage and in particular time intervals.
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Ganoderma Lucidum Protects Rat Brain Tissue Against Trauma-Induced Oxidative Stress
Özevren Hüseyin,İrtegün Sevgi,Deveci Engin,Aşır Fırat,Pektanç Gülsüm,Deveci Şenay 대한신경손상학회 2017 Korean Journal of Neurotrauma Vol.13 No.2
Objective: Traumatic brain injury causes tissue damage, breakdown of cerebral blood flow and metabolic regulation. Thisstudy aims to investigate the protective influence of antioxidant Ganoderma lucidum (G. lucidum) polysaccharides (GLPs)on brain injury in brain-traumatized rats. Methods: Sprague-Dawley conducted a head-traumatized method on rats by dropping off 300 g weight from 1 m height. Groups were categorized as control, G. lucidum, trauma, trauma+ G. lucidum (20 mL/kg per day via gastric gavage). Braintissues were dissected from anesthetized rats 7 days after injury. For biochemical analysis, malondialdehyde, glutathioneand myeloperoxidase values were measured. Results: In histopathological examination, neuronal damage in brain cortex and changes in blood brain barrier were observed. In the analysis of immunohistochemical and western blot, p38 mitogen-activated protein kinase, vascular endothelial growth factor and cluster of differentiation 68 expression levels were shown. These analyzes demonstrated the benefcial effects of GLPs on brain injury. Conclusion: We propose that GLPs treatment after brain injury could be an alternative treatment to decraseing inflammationand edema, preventing neuronal and glial cells degeneration if given in appropriate dosage and in particular time intervals.
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