Çetin A, Deveci E
Department of Neurosurgery, University of Health Sciences, Gazi Yaşargil Education and Research Hospital, Diyarbakır, Turkey.
Department of Histology and Embryology, Faculty of Medicine, Dicle University, Diyarbakır, Turkey.
Folia Morphol (Warsz). 2019;78(4):684-694. doi: 10.5603/FM.a2019.0029. Epub 2019 Mar 5.
Traumatic brain injury (TBI) leads to neuronal damage and neurological dysfunction. The aim of our study was to investigate the antioxidative effect of honokiol on TBI in rats with biochemical, histopathological and immunohistochemical methods.
Sprague-Dawley rats were subjected to TBI with a weight-drop device using 300 g/1 m weight/height impact. Forty-five rats were divided into three groups as control group, 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 analysed 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 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 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.
创伤性脑损伤(TBI)会导致神经元损伤和神经功能障碍。本研究旨在通过生化、组织病理学和免疫组织化学方法研究厚朴酚对大鼠创伤性脑损伤的抗氧化作用。
采用300 g/1 m重量/高度撞击的重物下落装置对Sprague-Dawley大鼠造成创伤性脑损伤。45只大鼠分为三组,即对照组、创伤性脑损伤组和创伤性脑损伤+厚朴酚组(5 mg/kg/天,腹腔注射)。创伤后7天,将溶解于二甲基亚砜(DMSO)的厚朴酚(5 mg/kg)腹腔注射给大鼠。实验结束时,采集动物血液样本并使用各种生化标志物进行分析。
创伤组的组织病理学检查显示一些锥体细胞变性、血管扩张和充血、内皮细胞增生、静脉周围炎症细胞浸润以及神经胶质延伸中断。在创伤性脑损伤+厚朴酚组中,锥体细胞变性减少,血管轻度扩张,内皮细胞向管腔方向改善,血管内炎症细胞减少。在创伤性脑损伤+厚朴酚组中,轻度扩张血管的内皮细胞和少数炎症细胞中血管内皮生长因子表达呈阳性。在创伤后血脑屏障受损的情况下,观察到创伤性脑损伤+厚朴酚组中神经胶质足突呈阳性表达并延伸至内皮细胞。
胶质纤维酸性蛋白表达在这些过程中呈阳性反应。考虑到抗氧化剂和炎症反应在创伤性颅脑损伤所致脑损伤中的重要作用,厚朴酚被认为在减少脂质过氧化、保护血脑屏障的膜结构、神经元和神经胶质细胞变性方面具有重要作用。