Farnesol quells oxidative stress, reactive gliosis and inflammation during acrylamide-induced neurotoxicity: Behavioral and biochemical evidence. (12th November 2015)

• Record Type: Journal Article
• Authors: Santhanasabapathy, R.; Vasudevan, S.; Anupriya, K.; Pabitha, R.; Sudhandiran, G.
• Is Part Of: Neuroscience. Volume 308(2015)
• Page Start: 212
• Page End: 227
• Publication Date: 2015-11-12
• Subjects: ACR Acrylamide -- AD Alzheimers disease -- ANOVA analysis of variance -- DAB Diaminobenzidine -- DPX di-n-butylphthalate-polystyrene-xylene -- GFAP Glial fibrillary acidic protein -- GSH glutathione -- HRP horse radish peroxidase -- IL-1β interleukin-1beta -- iNOS inducible form of nitric oxide synthase -- LPO lipid peroxidation -- LPS lipopolysaccharide -- MDA malondialdehyde -- NSE neuron-specific enolase -- PBS phosphate buffered saline -- ROS reactive oxygen species -- TBS Tris-buffered saline -- TNF-α tumor necrosis factor alpha; acrylamide -- farnesol -- oxidative stress -- neuroinflammation -- reactive gliosis -- neurodegeneration; Neurochemistry -- Periodicals; Neurophysiology -- Periodicals; Neurology -- Periodicals; Neurochimie -- Périodiques; Neurophysiologie -- Périodiques; Neurochemistry; Neurophysiology; Electronic journals; Periodicals; Electronic journals; 612.8
• DOI: 10.1016/j.neuroscience.2015.08.067
• Languages: English
• ISSNs: 0306-4522

Abstract

Graphical abstract: Highlights: Farnesol possesses neuroprotective efficacy against ACR-induced neurotoxicity. Farnesol alleviated ACR-induced oxidative stress. Farnesol mitigates ACR-induced reactive gliosis. Farnesol improves neuromuscular strength and motor coordination during ACR-induced neurotoxicity. Abstract: Acrylamide (ACR) is an industrial pollutant, to which humans are exposed through chemicals associated with day to day human life and contributes to neurological disorders. The role of reactive gliosis upon toxic insults remains paradoxical, and the immunomodulatory events during ACR intoxication remain obscure. In view of this, the present study investigated ACR-induced (20 mg/kg b.wt for 4 weeks) neurodegeneration in the context of oxidative stress and associated inflammatory events and the ability of farnesol, a sesquiterpene, to mitigate reactive gliosis in the brain of Swiss albino mice. Farnesol supplementation (100 mg/kg b.wt.) showed a marked improvement in gait performance, neuromuscular function and fine motor coordination and attenuated ACR-induced diminution in glutathione (GSH) with parallel reduction in lipid peroxidation (LPO), protein carbonyls, hydroxide, hydroperoxide and nitrite levels. Farnesol treatment significantly ameliorated ACR-mediated histological aberrations and reactive gliosis by downregulating Glial fibrillary acidic protein (GFAP) and Ionizsed calcium-binding adapter molecule-1 ​(Iba-1) in the cortex, hippocampus and striatum. Further, ACR stimulated increase in levels of pro-inflammatory cytokines such as tumor necrosis factor alpha (TNF-α), interleukin-1β (IL-1β) and inducible form of nitric oxide synthase (iNOS) were considerably decreased by farnesol. In conclusion, our findings indicate that farnesol exerts neuroprotective efficacy during ACR-induced neuropathology by suppressing reactive gliosis and associated inflammatory events.