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

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 2 h followed by reperfusion and the infarct size was determined by 2,3,5-triphenyltetrazolium chloride (TTC) staining 6 h, 24 h, 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-kappa B and TNF-alpha. Results: The NF-kappa B levels in ischemic brain tissue increased 6 h after reperfusion and the TNF-a levels increased at 24 h, both reached their peaks at day 3 then decreased gradually, but remained above the controls at day 7. Vinpocetine decreased the levels of NF-kappa B and TNF-alpha 24 h and 3 days after reperfusion. Conclusion: NF-kappa B and TNF-alpha is associated with changes in brain edema and infarct volume. Vinpocetine decreases the expression of NF-kappa B and TNF-alpha and inhibits the inflammatory response after cerebral ischemia-reperfusion. (C) 2014 Elsevier Ireland Ltd. All rights reserved.