Farnesol quells oxidative stress, reactive gliosis and inflammation during acrylamide-induced neurotoxicity: Behavioral and biochemical evidence.
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 (20mg/kgb.wt for 4weeks) 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 (100mg/kgb.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.
Department of Biochemistry, Cell Biology Laboratory, University of Madras, Guindy Campus, Chennai 600 025, Tamil nadu, India.
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Santhanasabapathy
Department of Biochemistry, Cell Biology Laboratory, University of Madras, Guindy Campus, Chennai 600 025, Tamil nadu, India.
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Vasudevan
Department of Biochemistry, Cell Biology Laboratory, University of Madras, Guindy Campus, Chennai 600 025, Tamil nadu, India.
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Anupriya
Department of Biochemistry, Cell Biology Laboratory, University of Madras, Guindy Campus, Chennai 600 025, Tamil nadu, India.
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Pabitha
Department of Biochemistry, Cell Biology Laboratory, University of Madras, Guindy Campus, Chennai 600 025, Tamil nadu, India. Electronic address: sudhandiran@yahoo.com.
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Sudhandiran
D020106:Acrylamide / Q000633:toxicity*; D000818:Animals; D002540:Cerebral Cortex / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology; D003342:Corpus Striatum / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology; D004195:Disease Models, Animal; D005204:Farnesol / Q000494:pharmacology*; D005911:Gliosis / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology; D006624:Hippocampus / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology; D053583:Interleukin-1beta / Q000378:metabolism; D015227:Lipid Peroxidation / Q000187:drug effects / Q000502:physiology; D008297:Male; D051379:Mice; D009069:Movement Disorders / Q000188:drug therapy / Q000473:pathology / Q000503:physiopathology; D019636:Neurodegenerative Diseases / Q000139:chemically induced / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology; D015213:Neuroimmunomodulation / Q000187:drug effects / Q000502:physiology; D018696:Neuroprotective Agents / Q000494:pharmacology*; D018384:Oxidative Stress / Q000187:drug effects* / Q000502:physiology; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
C587672:IL1B protein, mouse; D053583:Interleukin-1beta; D018696:Neuroprotective Agents; D014409:Tumor Necrosis Factor-alpha; D020106:Acrylamide; D005204:Farnesol
acrylamide; farnesol; neurodegeneration; neuroinflammation; oxidative stress; reactive gliosis