title: Resolvin D2 recovers neural injury by suppressing inflammatory mediators expression in lipopolysaccharide-induced Parkinson's disease rat model.
abstract: Activation of microglial cells have been treated as the main role in the pathogenesis of neuropathic inflammation and neurodegenerative disease, including Parkinson's disease (PD), prion disease and Alzheimer's disease (AD). Resolvin D2 (RvD2) is derived from omega-3 polyunsaturated fatty acid and performs potent anti-inflammatory and pro-resolution effects. Here we investigated the effects of intrathecal injection of RvD2 for substantia nigra pars compacta (SNpc) in vivo and primary microglia in vitro experiment on pro-inflammatory cytokine expression and NF-κB activation in Lipopolysaccharide (LPS)-induced PD rat model. The total of 30 days experimental period were used for the rats' experiment, the LPS-induced inflammation in SNpc increase the expression of NO, iNOS, TNF-α, IL-1, IL-18, IL-6, IL-1β, ROS production, the translocation of NF-κB p65, IκBα, and IKKβ expression in glial cells. After injection of RvD2, the treatment prevented development of behavioral defects and TLR4/NF-κB pathway activation. Therefore, we demonstrated a novel role of RvD2 in treatment of rat PD model and LPS activated microglia inflammation. Given the significant potency of RvD2 and well-known side effects of microglia inflammatory inhibitors, it may represent novel hotspot for treating neurodegenerative disease.
authors.affiliation: School of Pharmacy, Guangdong Food and Drug Vocational College, Guangzhou 510520, PR China. Electronic address: xukang316004@126.com.
authors.forename: Yuguang
authors.initials: Y
authors.lastname: Tian
authors.affiliation: School of Pharmacy, Guangdong Food and Drug Vocational College, Guangzhou 510520, PR China; Neuroscience Care Unit, The Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, Number 88, Jiefang Road, Hangzhou, Zhejiang 310009, PR China. Electronic address: zhangying310009@126.com.
authors.forename: Ying
authors.initials: Y
authors.lastname: Zhang
authors.affiliation: Department of Geriatrics, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Number 88, Jiefang Road, Hangzhou, Zhejiang 310009, PR China.
authors.forename: Ruoyu
authors.initials: R
authors.lastname: Zhang
authors.affiliation: Department of Neurology, Zhejiang Hospital, Number 12, Lingyin Road, Xihu District, Hangzhou, Zhejiang 310009, PR China.
authors.forename: Song
authors.initials: S
authors.lastname: Qiao
authors.affiliation: Neuroscience Care Unit, The Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, Number 88, Jiefang Road, Hangzhou, Zhejiang 310009, PR China.
authors.forename: Jing
authors.initials: J
authors.lastname: Fan
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D004281:Docosahexaenoic Acids / Q000502:physiology*; D004797:Enzyme-Linked Immunosorbent Assay; D018836:Inflammation Mediators / Q000378:metabolism*; D008070:Lipopolysaccharides / Q000494:pharmacology*; D008297:Male; D009474:Neurons / Q000473:pathology*; D010300:Parkinson Disease / Q000209:etiology / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D060888:Real-Time Polymerase Chain Reaction
chemical_list: D018836:Inflammation Mediators; D008070:Lipopolysaccharides; C545423:resolvin D2; D004281:Docosahexaenoic Acids
keywords: Neurodegenerative disease; Parkinson's disease; Resolvin D2; Substantia nigra pars compacta (SNpc)