title: [Role of free radicals in brain edema induced by endotoxin in infant rats and the therapeutic effect of dexamethasone and IVIG].
abstract: OBJECTIVE
  Glucocorticoid is considered as an effective drug for prevention and treatment of brain edema and reducing the blood-brain barrier (BBB) permeability. Intravenous immunoglobulin (IVIG) is frequently used to treat neurological diseases with immune abnormality, its function and potential mechanism on brain edema have not been reported. In this study, the roles of the total hydrosulfide group (TSH), non-protein hydrosulfide group (NPSH) and malondialdehyde (MDA) in etiology of the endotoxin brain edema in infant rats and the interfering effects of dexamethasone (DEX) and IVIG were investigated.
  
  
  METHODS
  In 35 infant rats, 10 mg/kg lipopolysaccharide (LPS) was intraperitoneally injected. The same volume of normal saline was injected to 24 control rats. Ten mg/kg DEX and 400 mg/kg IVIG were intravenously injected respectively to 36 and 24 infant rats instantly following LPS injection. The TSH, NPSH and MDA concentrations and the brain Evans blue contents were detected at different time in the brain tissue. The brain water content was measured by drying method.
  
  
  RESULTS
  The brain water, EB and MDA contents after endotoxin injection were significantly higher than those of control group, while the brain TSH, NPSH content were significantly lower than those of control group (P < 0.05 or P < 0.01); After treatment with DEX or IVIG, the brain EB, MDA and water content significantly decreased with the peak at 6 h (P < 0.05 or P < 0.01), TSH and NPSH significantly increased compared with LPS group. However, the NPSH content in IVIG treatment group did not change significantly (P > 0.05).
  
  
  CONCLUSIONS
  Free radicals play a role in the brain edema induced by LPS in infant rats. The primary results suggested that DEX and IVIG have therapeutic effect for the endotoxin-induced brain edema by affecting the free radicals.
authors.affiliation: Department of Neurology, Children's Hospital, Chongqing Medical University, Chongqing 400014, China.
authors.forename: Mei
authors.initials: M
authors.lastname: Li
authors.forename: Fang-cheng
authors.initials: FC
authors.lastname: Cai
mesh_terms: D000818:Animals; D001812:Blood-Brain Barrier / Q000187:drug effects / Q000378:metabolism; D001929:Brain Edema / Q000139:chemically induced / Q000188:drug therapy* / Q000378:metabolism; D003907:Dexamethasone / Q000627:therapeutic use*; D004731:Endotoxins / Q000633:toxicity*; D005609:Free Radicals / Q000032:analysis*; D005938:Glucocorticoids / Q000627:therapeutic use; D016756:Immunoglobulins, Intravenous / Q000008:administration & dosage / Q000627:therapeutic use*; D008315:Malondialdehyde / Q000032:analysis; D051381:Rats; D017208:Rats, Wistar; D013440:Sulfides / Q000032:analysis
chemical_list: D004731:Endotoxins; D005609:Free Radicals; D005938:Glucocorticoids; D016756:Immunoglobulins, Intravenous; D013440:Sulfides; D008315:Malondialdehyde; D003907:Dexamethasone