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首页> 外文期刊>Neuroscience Letters: An International Multidisciplinary Journal Devoted to the Rapid Publication of Basic Research in the Brain Sciences >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
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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

机译:长春西汀对大鼠脑缺血再灌注损伤模型中核因子-κB和肿瘤坏死因子-α功能表达的抗炎作用

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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 6h, 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-kappaB and TNF-alpha. Results: The NF-kappaB levels in ischemic brain tissue increased 6 h after reperfusion and the TNF-alpha 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-kappaB and TNF-alpha 24 h and 3 days after reperfusion. Conclusion: NF-kappaB and TNF-alpha is associated with changes in brain edema and infarct volume. Vinpocetine decreases the expression of NF-kappaB and TNF-alpha and inhibits the inflammatory response after cerebral ischemia-reperfusion.
机译:目的:缺血性中风后脑血流的恢复可防止进一步的广泛损害,但可能导致再灌注损伤。炎症反应是涉及脑缺血-再灌注损伤的许多因素之一。这项研究调查了长春西汀(一种用于治疗认知障碍的药物)的用途,以探讨其对大鼠脑缺血再灌注模型中炎症的影响。方法:Wistar大鼠随机分为对照组(n = 40),脑缺血再灌注组(n = 52)和长春西汀脑缺血再灌注组(n = 52)。诱导大脑中动脉闭塞模型2小时,然后再灌注,再灌注后6h,24 h,3天和7天,通过2,3,5-三苯基四唑氯化物(TTC)染色确定梗塞面积。干湿重法用于测量脑水含量并评估脑水肿程度。免疫组织化学和原位杂交技术检测NF-κB和TNF-α的表达。结果:缺血性脑组织中的NF-κB水平在再灌注后6 h升高,而TNF-α水平在24 h升高,均在第3天达到峰值,然后逐渐降低,但在第7天仍高于对照。再灌注后24小时和3天的NF-κB和TNF-α的水平。结论:NF-κB和TNF-α与脑水肿和梗死体积的改变有关。长春西汀降低了脑缺血再灌注后NF-κB和TNF-α的表达,并抑制了炎症反应。

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