title: Fucoidan protects against lipopolysaccharide-induced rat neuronal damage and inhibits the production of proinflammatory mediators in primary microglia.
abstract: BACKGROUND
  Fucoidan, a sulfated polysaccharide extracted from brown algae, possesses potent antiinflammatory effects.
  
  
  OBJECTIVE
  To examine the effect of fucoidan treatment on inflammation-mediated dopaminergic neuronal damage and its potential mechanisms.
  
  
  METHODS
  Microglial activation and injury of dopaminergic neurons were induced by intranigral injection of lipopolysaccharide (LPS), and the effects of fucoidan treatment on animal behavior, microglial activation and survival ratio of dopaminergic neurons were investigated. We further observed the efficacy of fucoidan on tumor necrosis factor-alpha (TNF-α) and the production of reactive oxygen species (ROS) in LPS-activated primary microglia.
  
  
  RESULTS
  Fucoidan significantly improved the behavioral manifestation, prevented the loss of dopaminergic neurons and inhibited the deleterious activation of microglia in the substantia nigra pars compacta of LPS-treated rats. Further in vitro experiments indicated that the excessive production of TNF-α and ROS in LPS-induced primary microglia were significantly inhibited by fucoidan administration.
  
  
  CONCLUSIONS
  This is the first study to demonstrate that fucoidan possesses neuroprotective effects on injured dopaminergic neurons in a LPS-induced animal model of Parkinson's disease. The mechanisms underlying these effects may include its potent down-regulation of intracellular ROS and subsequent proinflammatory cytokine release in LPS-activated microglia.
authors.affiliation: Capital Medical University Yanjing Medical College, Beijing, China; Key laboratory of Neurodegenerative Diseases of the Ministry of Education, Capital Medical University, Beijing, China.
authors.forename: Yan-Qiu
authors.initials: YQ
authors.lastname: Cui
authors.forename: Yan-Jun
authors.initials: YJ
authors.lastname: Jia
authors.forename: Ting
authors.initials: T
authors.lastname: Zhang
authors.forename: Quan-Bin
authors.initials: QB
authors.lastname: Zhang
authors.forename: Xiao-Min
authors.initials: XM
authors.lastname: Wang
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D001058:Apomorphine / Q000494:pharmacology; D001930:Brain Injuries / Q000139:chemically induced* / Q000150:complications / Q000517:prevention & control*; D039481:CD11b Antigen / Q000378:metabolism; D004195:Disease Models, Animal; D018491:Dopamine Agonists / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D004797:Enzyme-Linked Immunosorbent Assay; D008070:Lipopolysaccharides / Q000633:toxicity*; D008297:Male; D001523:Mental Disorders / Q000188:drug therapy / Q000209:etiology; D017628:Microglia / Q000187:drug effects / Q000378:metabolism*; D018696:Neuroprotective Agents / Q000627:therapeutic use*; D011134:Polysaccharides / Q000627:therapeutic use*; D051381:Rats; D017207:Rats, Sprague-Dawley; D017382:Reactive Oxygen Species / Q000378:metabolism; D013239:Stereotyped Behavior / Q000187:drug effects / Q000502:physiology; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism*; D014446:Tyrosine 3-Monooxygenase / Q000378:metabolism
chemical_list: D039481:CD11b Antigen; D018491:Dopamine Agonists; D008070:Lipopolysaccharides; D018696:Neuroprotective Agents; D011134:Polysaccharides; D017382:Reactive Oxygen Species; D014409:Tumor Necrosis Factor-alpha; C007789:fucoidan; D014446:Tyrosine 3-Monooxygenase; D001058:Apomorphine