Naringenin protects AlCl3/D-galactose induced neurotoxicity in rat model of AD via attenuation of acetylcholinesterase levels and inhibition of oxidative stress
Autoři:
Saida Haider aff001; Laraib Liaquat aff001; Saara Ahmad aff002; Zehra Batool aff001; Rafat Ali Siddiqui aff004; Saiqa Tabassum aff001; Sidrah Shahzad aff001; Sahar Rafiq aff001; Narjis Naz aff007
Působiště autorů:
Neurochemistry and Biochemical Neuropharmacology Research Unit, Department of Biochemistry, University of Karachi, Karachi, Pakistan
aff001; Department of Biological and Biomedical Sciences, The Aga Khan University, Karachi, Pakistan
aff002; Dr. Panjwani Center for Molecular Medicine and Drug Research, International Center for Chemical and Biological Sciences, University of Karachi, Karachi, Pakistan
aff003; Nutrition Science and Food Chemistry Laboratory, Agricultural Research Station, Virginia State University, Petersburg, United States of America
aff004; Department of Biosciences, Shaheed Zuifiqar Ali Bhutto Institute of Science and Technology, Karachi, Pakistan
aff005; Pakistan Navy Medical Training School and College, PNS Shifa, Karachi, Pakistan
aff006; Department of Genetics, University of Karachi, Karachi, Pakistan
aff007
Vyšlo v časopise:
PLoS ONE 15(1)
Kategorie:
Research Article
doi:
https://doi.org/10.1371/journal.pone.0227631
Souhrn
Currently prescribed medications for the treatment of Alzheimer’s disease (AD) that are based on acetylcholinesterase inhibition only offer symptomatic relief but do not provide protection against neurodegeneration. There appear to be an intense need for the development of therapeutic strategies that not only improve brain functions but also prevent neurodegeneration. The oxidative stress is one of the main causative factors of AD. Various antioxidants are being investigated to prevent neurodegeneration in AD. The objective of this study was to investigate the neuroprotective effects of naringenin (NAR) against AlCl3+D-gal induced AD-like symptoms in an animal model. Rats were orally pre-treated with NAR (50 mg/kg) for two weeks and then exposed to AlCl3+D-gal (150 mg/kg + 300 mg/kg) intraperitoneally for one week to develop AD-like symptoms. The standard drug, donepezil (DPZ) was used as a stimulator of cholinergic activity. Our results showed that NAR pre-treatment significantly protected AD-like behavioral disturbances in rats. In DPZ group, rats showed improved cognitive and cholinergic functions but the neuropsychiatric functions were not completely improved and showed marked histopathological alterations. However, NAR not only prevented AlCl3+D-gal induced AD-like symptoms but also significantly prevented neuropsychiatric dysfunctions in rats. Results of present study suggest that NAR may play a role in enhancing neuroprotective and cognition functions and it can potentially be considered as a neuroprotective compound for therapeutic management of AD in the future.
Klíčová slova:
Alzheimer's disease – Animal models – Antioxidants – Cognitive impairment – Hippocampus – Memory – Neurons – Rats
Zdroje
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