Neuroprotective effects of Syringic acid against aluminium chloride induced oxidative stress mediated neuroinflammation in rat model of Alzheimer's disease

Journal of Functional Foods

Thiyagarajan Ramesh¹  Vishnu Priya Veeraraghavan²  Xunyao Hou³  Yuanzheng Zhao⁴  Minyan Dang⁵  Wenzhi Zhang⁵  Yan Lei⁵ 

[1] Department of Basic Medical Sciences, College of Medicine, Prince Sattam Bin Abdulaziz University, Al-Kharj-11942, Saudi Arabia;Department of Biochemistry, Saveetha Dental College, Saveetha Institute of Medical and Technical Sciences, Saveetha University, Chennai 600 077, India;Department of Geriatric Neurology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong 250021, China;Department of Neurology, The Fifth Affiliated Hospital of Zhengzhou University, Zhengzhou city, Henan Province 450052, China;Innoscience Research Sdn Bhd, Jalan USJ 25/1, 47650 Subang Jaya, Selangor, Malaysia;

关键词: Alzheimer’s disease;    Aluminium chloride;    Syringic acid;    Neuroinflammation;    Oxidative stress;   

DOI  :  

来源: DOAJ

【 摘 要 】

Alzheimer’s disease (AD) is a major form of dementia among neurodegenerative diseases, which results in memory loss and attention deficits. Syringic acid (SA) is a phenolic compound derivative of plants and fruits, which possessed the numerous biological activities. The present study aims to examine the neuroprotective potential of SA on aluminium chloride (AlCl3) stimulated behavioral deficits and neuroinflammation in the rat AD. The AlCl3 (100 mg/kg.b.wt) via injected intraperitoneally for 60 days to stimulate the AD. The rats were supplemented with low and high doses of SA (25 & 50 mg/kg.b.wt) of SA for 30 days. After end of the experiment, we evaluated behavioral examinations like Morris water maze, Y-maze, elevated plus maze and open field test. Followed by acetylcholinesterase (AChE), biochemical measurement and inflammatory protein expression by western blotting were examined. AD rats displayed reduced memory and learning impairments, augmented short term memory loss and diminished locomotion activity. Interestingly, the neurobehavioral impairments were appreciably stabilized by the SA supplementation to the AD rats. The NF-ƙB, IL-1β, IL-6, and TNF-α expressions were assuaged via the SA supplementation to AD rats. The present work demonstrated that the SA treatment ameliorated the AlCl3 stimulated AD.

【 授权许可】

Unknown