title: Anti-inflammatory effects of vinpocetine on the functional expression of nuclear factor-kappa B and tumor necrosis factor-alpha in a rat model of cerebral ischemia-reperfusion injury.
abstract: OBJECTIVE
  The restoration of blood flow to the brain after ischemic stroke prevents further, extensive damage but can result in reperfusion injury. The inflammation response is one of many factors involved in cerebral ischemia-reperfusion injury. This study investigated the use of vinpocetine, a drug used to treat cognitive impairment, to explore its effects on inflammation in a rat model of cerebral ischemia-reperfusion.
  
  
  METHODS
  Wistar rats were randomly assigned to a control group, (n=40) a cerebral ischemia-reperfusion group (n=52) and a vinpocetine cerebral ischemia-reperfusion group (n=52). A model of middle cerebral artery occlusion was induced for 2h followed by reperfusion and the infarct size was determined by 2,3,5-triphenyltetrazolium chloride (TTC) staining 6h, 24h, 3 days, and 7 days after reperfusion. The dry-wet weight method was used to measure brain water content and evaluate the extent of brain edema. Immunohistochemistry and in-situ hybridization were used to detect the expression of NF-κB and TNF-α.
  
  
  RESULTS
  The NF-κB levels in ischemic brain tissue increased 6h after reperfusion and the TNF-α levels increased at 24h, both reached their peaks at day 3 then decreased gradually, but remained above the controls at day 7. Vinpocetine decreased the levels of NF-κB and TNF-α 24h and 3 days after reperfusion.
  
  
  CONCLUSIONS
  NF-κB and TNF-α is associated with changes in brain edema and infarct volume. Vinpocetine decreases the expression of NF-κB and TNF-α and inhibits the inflammatory response after cerebral ischemia-reperfusion.
authors.affiliation: Department of Neurology, Affiliated Fourth Centre Hospital of Tianjin Medical University, Tianjin 300140, China. Electronic address: wh1963919@163.com.
authors.forename: Hongxin
authors.initials: H
authors.lastname: Wang
authors.affiliation: Department of Neurology, Binzhou Medical University Hospitalbed, No. 661, Yellow-River Second Street, bed Shandong 256603, China.
authors.forename: Kan
authors.initials: K
authors.lastname: Zhang
authors.affiliation: Department of Neurology, Affiliated Fourth Centre Hospital of Tianjin Medical University, Tianjin 300140, China.
authors.forename: Lan
authors.initials: L
authors.lastname: Zhao
authors.affiliation: Department of Neurology, Affiliated Fourth Centre Hospital of Tianjin Medical University, Tianjin 300140, China.
authors.forename: Jiangwei
authors.initials: J
authors.lastname: Tang
authors.affiliation: Department of Neurology, Affiliated Fourth Centre Hospital of Tianjin Medical University, Tianjin 300140, China.
authors.forename: Luyan
authors.initials: L
authors.lastname: Gao
authors.affiliation: Department of Neurology, Affiliated Fourth Centre Hospital of Tianjin Medical University, Tianjin 300140, China.
authors.forename: Zhongping
authors.initials: Z
authors.lastname: Wei
mesh_terms: D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology* / Q000627:therapeutic use; D001929:Brain Edema / Q000188:drug therapy / Q000473:pathology; D020520:Brain Infarction / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology; D002545:Brain Ischemia / Q000188:drug therapy / Q000378:metabolism* / Q000473:pathology; D008297:Male; D016328:NF-kappa B / Q000378:metabolism*; D012333:RNA, Messenger / Q000378:metabolism; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000188:drug therapy / Q000378:metabolism* / Q000473:pathology; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism*; D014748:Vinca Alkaloids / Q000494:pharmacology* / Q000627:therapeutic use
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D016328:NF-kappa B; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D014748:Vinca Alkaloids; C013983:vinpocetine
keywords: Inflammation; NF-κB; Reperfusion injury; TNF-α; Vinpocetine