Allicin ameliorates aluminium- and copper-induced cognitive dysfunction in Wistar rats: relevance to neuro-inflammation, neurotransmitters and Aβ(1–42) analysis
- 22 May 2021
- journal article
- research article
- Published by Springer Science and Business Media LLC in JBIC Journal of Biological Inorganic Chemistry
- Vol. 26 (4), 495-510
- https://doi.org/10.1007/s00775-021-01866-8
Abstract
Alzheimer's disease (AD) is a multifactorial neurological disorder associated with neuropathological and neurobehavioral changes, like cognition and memory loss. Pathological hallmarks of AD comprise oxidative stress, formation of insoluble β-amyloid (Aβ) plaques, intracellular neurofibrillary tangles constituted by hyperphosphorylated tau protein (P-tau), neurotransmitters dysbalanced (DA, NE, 5-HT, GABA and Glutamate) and metal deposition. Chronic exposure to metals like aluminium and copper causes accumulation of Aβ plaques, promotes oxidative stress, neuro-inflammation, and degeneration of cholinergic neurons results in AD-like symptoms. In the present study, rats were administered with aluminium chloride (200 mg/kg p.o) and copper sulfate (0.5 mg/kg p.o) alone and in combination for 28 days. Allicin (10 and 20 mg/kg i.p) was administered from day 7 to day 28. Spatial and recognition memory impairment analysis was performed using Morris water maze, Probe trial, and Novel Object Recognition test. Animals were sacrificed on day 29, brain tissue was isolated, and its homogenate was used for biochemical (lipid peroxidation, nitrite, and glutathione), neuro-inflammatory (IL-1β, IL-6 and TNF- α), neurotransmitters (DA, NE, 5-HT, GABA and Glutamate), Aβ(1–42) level, Al concentration estimation, and Na+/K+-ATPase activity. In the present study, aluminium chloride and copper sulfate administration increased oxidative stress, inflammatory cytokines release, imbalanced neurotransmitters’ concentration, and promoted β-amyloid accumulation and Na+/K+-ATPase activity. Treatment with allicin dose-dependently attenuated these pathological events via restoration of antioxidants, neurotransmitters concentration, and inhibiting cytokine release and β-amyloid accumulation. Moreover, allicin exhibited the neuroprotective effect through antioxidant, anti-inflammatory, neurotransmitters restoration, attenuation of neuro-inflammation and β-amyloid-induced neurotoxicity.Keywords
This publication has 44 references indexed in Scilit:
- Chronic exposure to aluminum reduces tyrosine hydroxylase expression in the substantia nigra and locomotor performance in ratsNeuroscience Letters, 2011
- Non-Steroidal Anti-Inflammatory Drugs in Alzheimer's Disease and Parkinson's Disease: Reconsidering the Role of NeuroinflammationPharmaceuticals, 2010
- A Hundred Years of Alzheimer's Disease ResearchNeuron, 2006
- Aluminum and copper in drinking water enhance inflammatory or oxidative events specifically in the brainJournal of Neuroimmunology, 2006
- Simple and rapid determination of serotonin and catecholamines in biological tissue using high-performance liquid chromatography with electrochemical detectionJournal of Chromatography B, 2005
- An improved and rapid HPLC-EC method for the isocratic separation of amino acid neurotransmitters from brain tissue and microdialysis perfusatesLife Sciences, 1988
- A new one-trial test for neurobiological studies of memory in rats. 1: Behavioral dataBehavioural Brain Research, 1988
- Developments of a water-maze procedure for studying spatial learning in the ratJournal of Neuroscience Methods, 1984
- Selenium: Biochemical Role as a Component of Glutathione PeroxidaseScience, 1973
- Red cell and plasma cholinesterase activities in microsamples of human and animal blood determined simultaneously by a modified acetylthiocholine/DTNB procedureToxicology and Applied Pharmacology, 1970