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长春西汀对脑缺血/再灌注损伤的保护作用及机制研究 被引量:7

Protective effect and mechanism of vinpocetine on the cerebral ischemia/reperfusion injury
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摘要 目的探讨长春西汀对脑缺血/再灌注损伤的保护作用及发挥药效的机制。方法使用线拴法制备脑缺血/再灌注损伤模型,分为假手术组、预处理组和模型组,预处理组大鼠造模前按4 mg/(kg·d)剂量给予7 d长春西汀,其他组大鼠给予等剂量的生理盐水。对造模后各组大鼠脑含水量、神经功能缺损评分、脑梗死体积、高敏C反应蛋白(hs-CRP)、肿瘤坏死因子-α(TNF-α)、丙二醛(MDA)和超氧化物歧化酶(SOD)等指标进行检测。结果预处理组的脑含水量多于假手术组,模型组的脑含水量多于预处理组,差异均有统计学意义(P<0.05);模型组的神经功能缺失症状评分、脑梗死体积与预处理组比较,差异有统计学意义(P<0.05);假手术组、预处理组和模型组的hs-CRP、TNF-α及MDA水平依次升高,SOD水平依次降低,差异均有统计学意义(P<0.05)。结论长春西汀对脑缺血/再灌注损伤具有保护作用,后者可能是通过调节炎症反应和自由基而实现的。 Objective To investigate the protective effect and the mechanism of vinpocetine on cerebral ischemia / reperfusion injury. Methods The cerebral ischemia / reperfusion injury model was prepared by suture method,and the model rats were divided into sham operation group,pre-treatment group and model group. Pre-treatment group rats were pretreated before modeling by vinpocetine 4 mg /( kg·d),rats in another groups received the same dose of saline.The water content of brain,nerve function deficiency symptom score,cerebral infarction volume,high sensitive C reactive protein( hs-CRP),tumor necrosis factor alpha( TNF-α),malondialdehyde( M DA) and superoxide dismutase( SOD)were detected. Results The water content of brain: model group pre-treatment group sham operation group( P〈0. 05). There were significant differences in the neurological severity score and infarct volume between pre-treatment group and model group( P〈0. 05). The levels of hs-CRP,TNF-α and M DA: model group pre-treatment group sham operation group( P〈0. 05); the level of SOD: model group pre-treatment group sham operation group( P〈0. 05).Conclusion Vinpocetine has protective effect on cerebral ischemia / reperfusion injury by modulating the inflammatory reaction and free radical.
作者 苏文生
出处 《实用药物与临床》 CAS 2015年第6期656-658,共3页 Practical Pharmacy and Clinical Remedies
关键词 脑缺血/再灌注 长春西汀 炎症反应 自由基 Cerebral ischemia / reperfusion Vinpocetine Inflammatory reaction Free radical
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