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作 者:王红柏[1] 王海云[1] 王国林[1] 朱爱[1] 刘书颖
机构地区:[1]天津医科大学总医院麻醉科天津市麻醉学研究所,300052
出 处:《中华麻醉学杂志》2014年第10期1181-1184,共4页Chinese Journal of Anesthesiology
基 金:国家自然科学基金(81071059,81100984);天津市卫生局科技基金(09KZ106)
摘 要:目的 评价异丙酚后处理对脑缺血再灌注损伤大鼠海马神经元K+-Cl-共转运体2(KCC2)表达的影响.方法 SD雄性大鼠72只,7~8周龄,体重250 ~ 280 g,采用随机数字表法,将其分为3组(n=24):假手术组(S组)、缺血再灌注组(I/R组)和异丙酚后处理组(PP组).采用阻塞大脑中动脉的方法制备大鼠脑缺血再灌注损伤模型,PP组于再灌注即刻开始静脉输注异丙酚20mg· kg^-1·h^-1,输注时间2h,S组和I/R组输注等容量生理盐水.于再灌注24h时行改良神经功能缺损程度评分(mNSS),然后取脑组织,尼氏染色,进行海马CA3区神经元计数;采用免疫荧光法和Western blot法检测海马CA3区KCC2表达水平.结果 与S组比较,I/R组mNSS评分升高,海马CA3区神经元计数和KCC2表达降低,PP组mNSS评分升高(P<0.05),PP组其它指标差异无统计学意义(P>0.05);与I/R组比较,PP组mNSS评分降低,海马CA3区神经元计数和KCC2表达升高(P<0.05).结论 异丙酚后处理减轻大鼠脑缺血再灌注损伤的机制与上调海马神经元KCC2表达有关.Objective To evaluate the effect of propofol post-conditioning on hippocampal neuronal K+ - Cl- co-transporter 2 (KCC2) expression in the rats with cerebral ischemia/reperfusion (I/R) injury. Methods Seventy-two male Sprague-Dawley rats, aged 7-8 weeks, weighing 250-280 g, were randomly divided into 3 groups (n = 24 each): sham operation group (group S), cerebral I/R (group l/R) and propofol post-conditioning group (group PP). The model of focal cerebral I/R injury was established by occlusion of the right middle cerebral artery. Propofol 20 mg kg^- 1 h^- 1 was infused over 2 h starting from the onset of reperfusion through the femoral vein in group PP. The equal volume of normal saline was given in S and I/R groups. Modified neurological severity score (mNSS) was used to evaluate the impairment of neurological function. The animals were then sacrificed and brains were removed for determination of the number of neurons (by Nissl' s staining) and expression of KCC2 (by immunofluoreseence and Western blot) in hippocampal CA3 region. Results Compared with group S, the scores of mNSS were significantly increased, and the number of neurons and expression of KCC2 in hippocampal CA3 region were decreased in I/R group, and mNSS scores were increased, and no significant changes were found in the other parameters in group PP. Compared with group I/R, the mNSS scores were significantly decreased, and the number of neurons and expression of KCC2 in hippocampal CA3 region were increased in group PP. Conclusion The mechanism by which propofol post-conditioning reduces cerebral I/R injury is related to up-regulated expressionof hippocampal KCC2 in rats.
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