Akinmoladun Afolabi C, Akinrinola Bolanle L, Olaleye M Tolulope, Farombi Ebenezer O
Department of Biochemistry, The Federal University of Technology, School of Sciences, Akure, Nigeria,
Neurochem Res. 2015 Apr;40(4):777-87. doi: 10.1007/s11064-015-1527-z. Epub 2015 Feb 1.
The pathophysiology of stroke is characterized by biochemical and physical alterations in the brain. Modulation of such aberrations by therapeutic agents affords insights into their mechanism of action. Incontrovertible evidences that oxidative stress is involved in the pathophysiology of neurologic disorders have brought antioxidative compounds, especially plant phytochemicals, under increasing focus as potential remedies for the prevention and management of neurodegenerative diseases. Kolaviron, a biflavonoid complex isolated from Garcinia kola Heckel (Guttiferae) was evaluated for neuroprotectivity in brains of male Wistar rats submitted to bilateral common carotid artery occlusion-induced global ischemia/reperfusion injury (I/R). Animals were divided into six groups: sham treated, vehicle (I/R), 50 mg/kg kolaviron + I/R, 100 mg/kg kolaviron + I/R, 200 mg/kg kolaviron + I/R and quercetin (20 mg/kg i.p.) + I/R. The common carotid arteries were occluded for 30 min followed by 2 h of reperfusion. Relative brain weight and brain water content were determined and oxidative stress and neurochemical markers were also evaluated. I/R caused significant decreases in glutathione level and the activities of enzymic antioxidants, the sodium pump and acetylcholinesterase while significant increases were recorded in relative brain weight, brain water content, lipid peroxidation and the activities of glutamine synthetase and myeloperoxidase. There was a remarkable ablation of I/R induced oxidative stress, neurochemical aberrations and brain edema in animals pretreated with kolaviron. The results suggested that the protection afforded by kolaviron probably involved regulation of redox and electrolyte homeostasis as well as anti-inflammatory and antiexcitotoxic mechanisms.
中风的病理生理学特征是大脑中的生化和物理改变。治疗药物对这些异常的调节有助于深入了解其作用机制。氧化应激参与神经疾病病理生理学的无可争议的证据,使抗氧化化合物,尤其是植物化学物质,作为预防和治疗神经退行性疾病的潜在药物受到越来越多的关注。对从可乐果(藤黄科)中分离出的双黄酮复合物可乐维纶,在接受双侧颈总动脉闭塞诱导的全脑缺血/再灌注损伤(I/R)的雄性Wistar大鼠脑中的神经保护作用进行了评估。动物分为六组:假手术组、溶剂对照组(I/R)、50mg/kg可乐维纶+I/R组、100mg/kg可乐维纶+I/R组、200mg/kg可乐维纶+I/R组和槲皮素(20mg/kg腹腔注射)+I/R组。颈总动脉闭塞30分钟,随后再灌注2小时。测定相对脑重量和脑含水量,并评估氧化应激和神经化学标志物。I/R导致谷胱甘肽水平和酶抗氧化剂、钠泵及乙酰胆碱酯酶活性显著降低,而相对脑重量、脑含水量、脂质过氧化以及谷氨酰胺合成酶和髓过氧化物酶活性显著增加。用可乐维纶预处理的动物中,I/R诱导的氧化应激、神经化学异常和脑水肿有明显减轻。结果表明,可乐维纶提供的保护作用可能涉及氧化还原和电解质稳态的调节以及抗炎和抗兴奋毒性机制。