title: n-3 polyunsaturated fatty acids inhibit lipopolysaccharide-induced microglial activation and dopaminergic injury in rats.
abstract: Increasing evidence indicates that neuroinflammation plays an important role in neurotoxins-induced neurodegenerations. Microglia are a type of glial cells in the brain and play as the first and main form of active immune defense in the central nervous system. Accumulated data suggest that the activation of microglia plays a critical role in neurotoxicities induced by environmental toxicants. So the inhibition of microglia has been proven to be an effective strategy against neurotoxic effects. In the present study, we found that n-3 polyunsaturated fatty acids can inhibit both microglial activation and dopaminergic injury in the substantia nigra of Sprague-Dawley rats induced by lipopolysaccharide, one of the major constituents of the outer membrane of Gram-negative bacteria. Moreover, n-3 polyunsaturated fatty acids inhibited lipopolysaccharide-induced activation of nuclear factor-κB, an important transcription factor involved in microglial activation. Taken together, our results provided the first in vivo evidence that n-3 polyunsaturated fatty acids can inhibit the damage of dopaminergic neurons induced by lipopolysaccharide through their inhibitory effects on nuclear factor-κB-dependent microglial activation.
authors.affiliation: Department of Nutrition & Food Hygiene and the Ministry of Education Key Lab of Hazard Assessment and Control in Special Operational Environment, School of Public Health, Fourth Military Medical University, Xi'an 710032, China.
authors.forename: Ailing
authors.initials: A
authors.lastname: Ji
authors.forename: Huan
authors.initials: H
authors.lastname: Diao
authors.forename: Xiaohui
authors.initials: X
authors.lastname: Wang
authors.forename: Ruihua
authors.initials: R
authors.lastname: Yang
authors.forename: Jianbin
authors.initials: J
authors.lastname: Zhang
authors.forename: Wenjing
authors.initials: W
authors.lastname: Luo
authors.forename: Rui
authors.initials: R
authors.lastname: Cao
authors.forename: Zipeng
authors.initials: Z
authors.lastname: Cao
authors.forename: Feng
authors.initials: F
authors.lastname: Wang
authors.forename: Tongjian
authors.initials: T
authors.lastname: Cai
mesh_terms: D000818:Animals; D001522:Behavior, Animal / Q000187:drug effects; D019610:Cytoprotection; D004195:Disease Models, Animal; D004281:Docosahexaenoic Acids / Q000494:pharmacology*; D059290:Dopaminergic Neurons / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D015118:Eicosapentaenoic Acid / Q000494:pharmacology*; D008070:Lipopolysaccharides; D008297:Male; D017628:Microglia / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D009043:Motor Activity / Q000187:drug effects; D016328:NF-kappa B / Q000378:metabolism; D009410:Nerve Degeneration; D018696:Neuroprotective Agents / Q000494:pharmacology*; D020734:Parkinsonian Disorders / Q000139:chemically induced / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013378:Substantia Nigra / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D014446:Tyrosine 3-Monooxygenase / Q000378:metabolism
chemical_list: D008070:Lipopolysaccharides; D016328:NF-kappa B; D018696:Neuroprotective Agents; D004281:Docosahexaenoic Acids; D015118:Eicosapentaenoic Acid; D014446:Tyrosine 3-Monooxygenase