Chen Xiao, Zhang Min, Ahmed Mukhtar, Surapaneni Krishna Mohan, Veeraraghavan Vishnu Priya, Arulselvan Palanisamy
Second Department of Encephalopathy, Xi'an Encephalopathy Hospital of Traditional Chinese Medicine, 710032 Xi'an, Shaanxi, China.
Department of Zoology, College of Science, King Saud University, Riyadh, Saudi Arabia.
Saudi J Biol Sci. 2021 Aug;28(8):4232-4239. doi: 10.1016/j.sjbs.2021.06.031. Epub 2021 Jun 15.
Alzheimer's disease (AD) is a chronic neurodegenerative disease categorized by the deficiency in the cognition and memory. Approximately 50 million peoples has the AD, which is categorized by the deficiency in the cognition, memory and other kinds of cognitive dissention. The present exploration was designed to unveil the ameliorative properties of ononin against the aluminium chloride (AlCl3)-provoked AD in animals via the suppression of oxidative stress and neuroinflammation. AD was provoked to the Sprague Dawley rats through administering orally with 0.5 ml/100 g b.wt. of AlCl3 25 days and then supplemented with the 30 mg/kg of ononin orally for 25th day to 36th day. The behavioural changes were examined using open field and Morris Water Maze test. The acetylcholine esterase (AChE) activity was studied by standard method. The status of Aβ1-42, MDA, SOD, total antioxidant capacity (TAC) were quantified using respective assay kits. The interleukin(IL)-1β and TNF-α, BDNF, PPAR-γ, p38MAPK, and NF-κB/p65 status was quantified using respective assay kits. Brain histology was studied using microscope. The ononin treatment effectively modulated the AlCl3-triggered behavioural alterations in the AD animals. Ononin appreciably suppressed the AChE, Aβ1-42, and MDA and improved the SOD and TAC in the brain tissues of AD animals. The status of IL-1β, TNF-α, p38MAPK, and NF-κB were suppressed and the BDNF and PPAR-γ contents were elevated in the brain tissues of AD animals. The outcomes brain histology analysis proved the attenuate role of ononin. Our findings recommended that the ononin treatment could ameliorate the cognitive impairment, suppress the neuroinflammation and oxidative stress in the AD animals.
阿尔茨海默病（AD）是一种以认知和记忆缺陷为特征的慢性神经退行性疾病。约5000万人患有AD，其特征为认知、记忆及其他各类认知障碍。本研究旨在通过抑制氧化应激和神经炎症，揭示鹰嘴豆芽素A对动物氯化铝（AlCl3）诱发的AD的改善作用。通过给Sprague Dawley大鼠口服0.5 ml/100 g体重的AlCl3，持续25天，诱发AD，然后从第25天至第36天口服补充30 mg/kg的鹰嘴豆芽素A。使用旷场试验和莫里斯水迷宫试验检测行为变化。采用标准方法研究乙酰胆碱酯酶（AChE）活性。使用相应试剂盒对Aβ1-42、丙二醛（MDA）、超氧化物歧化酶（SOD）、总抗氧化能力（TAC）进行定量。使用相应试剂盒对白细胞介素（IL）-1β、肿瘤坏死因子-α、脑源性神经营养因子（BDNF）、过氧化物酶体增殖物激活受体-γ（PPAR-γ）、p38丝裂原活化蛋白激酶（p38MAPK）和核因子-κB/p65状态进行定量。使用显微镜研究脑组织学。鹰嘴豆芽素A治疗有效调节了AD动物中AlCl3引发的行为改变。鹰嘴豆芽素A显著抑制了AD动物脑组织中的AChE、Aβ1-42和MDA，并提高了SOD和TAC。AD动物脑组织中IL-1β、TNF-α、p38MAPK和NF-κB的状态受到抑制，BDNF和PPAR-γ含量升高。脑组织学分析结果证明了鹰嘴豆芽素A的减轻作用。我们的研究结果表明，鹰嘴豆芽素A治疗可改善AD动物的认知障碍，抑制神经炎症和氧化应激。
