Özevren Hüseyin, İrtegün Sevgi, Deveci Engin, Aşır Fırat, Pektanç Gülsüm, Deveci Şenay
Department of Neurosurgery, Faculty of Medicine, Dicle University, Diyarbakır, Turkey.
Department of Medical Biology, Faculty of Medicine, Dicle University, Diyarbakır, Turkey.
Korean J Neurotrauma. 2017 Oct;13(2):76-84. doi: 10.13004/kjnt.2017.13.2.76. Epub 2017 Oct 31.
Traumatic brain injury causes tissue damage, breakdown of cerebral blood flow and metabolic regulation. This study aims to investigate the protective influence of antioxidant () polysaccharides (GLPs) on brain injury in brain-traumatized rats.
Sprague-Dawley conducted a head-traumatized method on rats by dropping off 300 g weight from 1 m height. Groups were categorized as control, , trauma, trauma+ (20 mL/kg per day via gastric gavage). Brain tissues were dissected from anesthetized rats 7 days after injury. For biochemical analysis, malondialdehyde, glutathione and myeloperoxidase values were measured.
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 beneficial effects of GLPs on brain injury.
We propose that GLPs treatment after brain injury could be an alternative treatment to decraseing inflammation and edema, preventing neuronal and glial cells degeneration if given in appropriate dosage and in particular time intervals.
创伤性脑损伤会导致组织损伤、脑血流中断和代谢调节紊乱。本研究旨在探讨抗氧化剂()多糖(GLPs)对脑外伤大鼠脑损伤的保护作用。
采用从1米高度掉落300克重物的方法对Sprague-Dawley大鼠进行头部创伤。将大鼠分为对照组、、创伤组、创伤+(每天经胃灌胃20毫升/千克)。在损伤7天后,从麻醉的大鼠身上取出脑组织。进行生化分析时,测量丙二醛、谷胱甘肽和髓过氧化物酶的值。
在组织病理学检查中,观察到大脑皮质的神经元损伤和血脑屏障的变化。在免疫组织化学和蛋白质印迹分析中,显示了p38丝裂原活化蛋白激酶、血管内皮生长因子和分化簇68的表达水平。这些分析证明了GLPs对脑损伤的有益作用。
我们提出,脑损伤后给予GLPs治疗,如果给予适当剂量并在特定时间间隔内,可能是减少炎症和水肿、预防神经元和神经胶质细胞变性的一种替代治疗方法。