title: Oxidative stress induced by lipid peroxidation is related with inflammation of demyelination and neurodegeneration in multiple sclerosis.
abstract: BACKGROUND
  Multiple sclerosis (MS) is a chronic autoimmune demyelination disorder of the central nervous system (CNS) and its etiology remains unknown. The inflammatory environment in demyelinating lesions leads to the generation of oxygen- and nitrogen-free radicals as well as proinflammatory cytokines, which contribute to the development and progression of multiple sclerosis. Inflammation can lead to oxidative stress and vice versa. Thus, oxidative stress is involved in the inflammation leading demyelination and neurodegeneration in the pathogenesis of multiple sclerosis.
  
  
  CONCLUSIONS
  The present study aims to determine two biochemical markers of oxidative stress: TAC and MDA and to show their correlations whether oxidative stress reaction occurs in the demyelination through analyzing samples including peripheral blood and cerebrospinal fluid (CSF) from patients with relapsing-remitting MS (RR-MS). Totally, there were 20 patients in the control groups made from individuals with normal pressure hydrocephalus. Thirty MS patients diagnosed with McDonald diagnostic criteria (2010) treated with methylprednisolone were included in this study. Data were stratified by the degree of severity in order to clarify the role of oxidative stress in the mechanisms of MS and to assess its potential as a biomarker. Thirty clinically definite RRMS patients were enrolled in this study. Levels of MDA, GSH, total antioxidant capacity TAC, GSH-Px and ROS, were determined in serum of the control group and RRMS patients in 7 days before MP (methylprednisolone) treatment and one month after MP treatment. Statistical analysis was performed with one-way analysis of variance (ANOVA), followed by LSD's post hoc tests.
  
  
  CONCLUSIONS
  Oxidative stress precedes the inflammatory response in the multiple sclerosis patients. And methylprednisolone treatment can decrease brain antioxidant enzymes to reduce the neuroinflammatory attack.
authors.forename: Pin
authors.initials: P
authors.lastname: Wang
authors.forename: Keqin
authors.initials: K
authors.lastname: Xie
authors.forename: Cunfu
authors.initials: C
authors.lastname: Wang
authors.forename: Jianzhong
authors.initials: J
authors.lastname: Bi
mesh_terms: D000328:Adult; D000368:Aged; D000704:Analysis of Variance; D000975:Antioxidants / Q000378:metabolism; D002784:Cholesterol / Q000097:blood; D004185:Disability Evaluation; D005978:Glutathione / Q000097:blood; D006801:Humans; D015227:Lipid Peroxidation / Q000502:physiology*; D008775:Methylprednisolone / Q000134:cerebrospinal fluid; D008875:Middle Aged; D009103:Multiple Sclerosis / Q000134:cerebrospinal fluid / Q000150:complications*; D019636:Neurodegenerative Diseases / Q000134:cerebrospinal fluid / Q000209:etiology*; D018384:Oxidative Stress / Q000502:physiology*; D017382:Reactive Oxygen Species / Q000097:blood
chemical_list: D000975:Antioxidants; D017382:Reactive Oxygen Species; D002784:Cholesterol; D005978:Glutathione; D008775:Methylprednisolone