title: Oxymatrine reduces neuronal cell apoptosis by inhibiting Toll-like receptor 4/nuclear factor kappa-B-dependent inflammatory responses in traumatic rat brain injury.
abstract: OBJECTIVE
  To investigate the influence of oxymatrine (OMT) on Toll-like receptor 4 (TLR-4)/nuclear factor kappa-B (NF-κB)-dependent inflammatory responses and neuronal cell apoptosis after traumatic brain injury (TBI).
  
  
  METHODS
  Wistar rats were given an intraperitoneal injection of 60 or 120 mg/kg OMT after TBI once a day till day 5. Rats were killed by decapitation at hours 2, 6 and 12, and days 1, 2, 3 and 5 after TBI. Gene expressions of TLR-4 and NF-κB, concentrations of tumor necrosis factor-alpha (TNF-α), interleukin-1beta (IL-1β) and interleukin-6 (IL-6) as well as the number of apoptotic neuronal cells in traumatic rat brain tissues were determined.
  
  
  RESULTS
  The administration of 120 mg/kg OMT could significantly suppress gene expressions of TLR-4 and NF-κB, lessen concentrations of TNF-α, IL-1β and IL-6, and reduce the number of apoptotic neuronal cells in traumatic rat brain tissues by the Mann-Whitney U test (P < 0.05), but the administration of 60 mg/kg OMT could not (P > 0.05).
  
  
  CONCLUSIONS
  OMT may inhibit TLR4/NF-κB-dependent inflammatory responses, and furthermore lessen neuronal cell apoptosis after TBI.
authors.affiliation: Department of Neurosurgery, The First Hangzhou Municipal People's Hospital, Nanjing Medical University, 261 Huansha Road, Hangzhou, 310000, China. dxqhyy@163.com
authors.forename: Xiao-Qiao
authors.initials: XQ
authors.lastname: Dong
authors.forename: Wen-Hua
authors.initials: WH
authors.lastname: Yu
authors.forename: Yue-Yu
authors.initials: YY
authors.lastname: Hu
authors.forename: Zu-Yong
authors.initials: ZY
authors.lastname: Zhang
authors.forename: Man
authors.initials: M
authors.lastname: Huang
mesh_terms: D000470:Alkaloids / Q000494:pharmacology* / Q000627:therapeutic use; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology* / Q000627:therapeutic use; D017209:Apoptosis / Q000187:drug effects; D001930:Brain Injuries / Q000188:drug therapy / Q000378:metabolism*; D015870:Gene Expression / Q000187:drug effects; D007249:Inflammation / Q000188:drug therapy / Q000378:metabolism; D053583:Interleukin-1beta / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism; D008297:Male; D016328:NF-kappa B / Q000037:antagonists & inhibitors* / Q000235:genetics; D009474:Neurons / Q000187:drug effects / Q000378:metabolism; D011807:Quinolizines / Q000494:pharmacology* / Q000627:therapeutic use; D051381:Rats; D017208:Rats, Wistar; D051197:Toll-Like Receptor 4 / Q000037:antagonists & inhibitors* / Q000235:genetics; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D000093842:Matrines
chemical_list: D000470:Alkaloids; D000893:Anti-Inflammatory Agents; D053583:Interleukin-1beta; D015850:Interleukin-6; D016328:NF-kappa B; D011807:Quinolizines; D051197:Toll-Like Receptor 4; D014409:Tumor Necrosis Factor-alpha; C495347:Tlr4 protein, rat; C037573:oxymatrine; D000093842:Matrines