Liaquat Laraib, Ahmad Saara, Sadir Sadia, Batool Zehra, Khaliq Saima, Tabassum Saiqa, Emad Shaista, Madiha Syeda, Shahzad Sidrah, Haider Saida
Neurochemistry and Biochemical Neuropharmacology Research Unit, Department of Biochemistry, University of Karachi, Karachi, Pakistan.
Department of Biological and Biomedical Sciences, The Aga Khan University, Karachi, Pakistan.
Pak J Pharm Sci. 2017 Mar;30(2(Suppl.)):647-653.
Alzheimer's disease (AD) is an age-related neurodegenerative disorder associated with neurochemical and neurobehavioural alterations. Aluminium (Al) is considered as a contributing factor in the etiology of several neurodegenerative disorders like AD. D-galactose (D-gal) is a physiological nutrient but over supply induces some neurochemical and biochemical changes that exacerbate natural aging process. In this study, we aimed to develop AD animal model by co-administration of Al and D-gal in rats. Male albino Wistar rats were intraperitoneally injected with AlCl and D-gal at a dose of 150mg/kg and 300mg/kg respectively for one week. After one week rats were subjected to behavioural analysis. After behavioural analysis rats were decapitated to remove their brain. Biochemical and neurochemical analysis were conducted in whole brain. AlCl+D-gal significantly induced depressive and anxious behaviour in rats. Rats cognitive abilities were also significantly impaired following AlCl and D-gal co-administration. AlCl+D-gal significantly altered antioxidant enzyme activities and biogenic amine levels in whole brain. A marked increase in brain lipid peroxidation and acetylcholinesterase activity was found in test rats. These findings suggest that co-administration of AlCl3 and D-gal for one week could induce AD like symptoms and may be used to develop AD animal model.
阿尔茨海默病（AD）是一种与年龄相关的神经退行性疾病，伴有神经化学和神经行为改变。铝（Al）被认为是包括AD在内的几种神经退行性疾病病因中的一个促成因素。D-半乳糖（D-gal）是一种生理营养素，但过量供应会引发一些神经化学和生物化学变化，加剧自然衰老过程。在本研究中，我们旨在通过在大鼠中联合给予铝和D-半乳糖来建立AD动物模型。雄性白化Wistar大鼠分别以150mg/kg和300mg/kg的剂量腹腔注射氯化铝和D-半乳糖，持续一周。一周后对大鼠进行行为分析。行为分析后，将大鼠断头以取出其大脑。对全脑进行生化和神经化学分析。氯化铝+D-半乳糖显著诱导大鼠出现抑郁和焦虑行为。联合给予氯化铝和D-半乳糖后，大鼠的认知能力也显著受损。氯化铝+D-半乳糖显著改变了全脑中抗氧化酶活性和生物胺水平。在受试大鼠中发现脑脂质过氧化和乙酰胆碱酯酶活性显著增加。这些发现表明，联合给予氯化铝和D-半乳糖一周可诱导出类似AD的症状，可用于建立AD动物模型。
