Neuroprotective effect of hesperidin on aluminium chloride induced Alzheimer's disease in Wistar rats

• Published in: Neurochemical research Vol. 40; no. 4; pp. 767 - 776
• Main Authors: Justin Thenmozhi, Arokiasamy, Raja, Tharsius Raja William, Janakiraman, Udaiyappan, Manivasagam, Thamilarasan
• Format: Journal Article
• Language: English
• Published: United States Springer Nature B.V 01.04.2015
• Subjects: Acetylcholinesterase; Aluminum; Aluminum Chloride; Aluminum Compounds - toxicity; Alzheimer Disease - chemically induced; Alzheimer Disease - prevention & control; Alzheimer's disease; Amyloid precursor protein; Amyloidogenesis; Animals; Behavior, Animal; Body weight; Brain; Chemical synthesis; Chlorides; Chlorides - toxicity; Cortex; Field tests; Hesperidin; Hesperidin - pharmacology; Hippocampus; Injection; Intoxication; Male; Maze learning; Neurodegenerative diseases; Neuroprotection; Neuroprotective Agents - pharmacology; Open-field behavior; Proteins; Rats; Rats, Wistar; Rodents; Toxicity
• ISSN: 0364-3190; 1573-6903; 1573-6903
• DOI: 10.1007/s11064-015-1525-1

The present study was aimed to evaluate the protective effect of hesperidin (Hes) on aluminium chloride (AlCl3) induced neurobehavioral and pathological changes in Alzheimeric rats. Intraperitonial injection of AlCl3 (100 mg/kg body weight) for 60 days significantly elevated the levels of aluminium (Al), activity of acetylcholinesterase (AChE) and protein expressions of amyloid precursor protein (APP), β amyloid (Aβ 1-42), β and γ secretases as compared to control group in hippocampus and cortex of rat brain. Hes administration orally along with AlCl3 injection for 60 days, significantly revert the Al concentration, AChE activity and Aβ synthesis-related molecules in the studied brain regions. Our results showed that aluminum exposure was significantly reduced the spontaneous locomotor and exploratory activities in open field test and enhanced the learning and memory impairments in morris water maze test. The behavioral impairments caused by aluminum were significantly attenuated by Hes. The histopathological studies in the hippocampus and cortex of rat brain also supported that Hes (100 mg/kg) markedly reduced the toxicity of AlCl3 and preserved the normal histoarchitecture pattern of the hippocampus and cortex. From these results, it is concluded that hesperidin can reverse memory loss caused by aluminum intoxication through attenuating AChE activity and amyloidogenic pathway.