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作 者:赵杰 万海方[1] 汪国香[1] 傅云斌[1] 张燕
机构地区:[1]浙江省中西医结合医院麻醉科,杭州市310003
出 处:《中华麻醉学杂志》2017年第8期1013-1016,共4页Chinese Journal of Anesthesiology
摘 要:目的评价浅低温对脑缺血再灌注小鼠海马磷酸化真核翻译起始因子2α(p-eIf2α)表达的影响。方法清洁级健康雄性C57BL6小鼠60只,8~12周龄,体重20~30 g,采用随机数字表法分为3组(n=20):假手术组(S组)、脑缺血再灌注组(I/R组)和浅低温组(H组)。采用阻断双侧颈总动脉15 min后恢复灌注的方法制备小鼠脑缺血再灌注损伤模型。H组再灌注即刻小鼠全身喷洒酒精行体表降温,维持直肠温度32~34 ℃,持续3 h。于再灌注24 h时进行神经功能缺陷评分。随后处死小鼠取海马,观察海马CA1区病理学结果,采用TUNEL法检测神经元凋亡情况,计算神经元凋亡率,采用Western blot法检测p-eIf2α的表达。结果与S组比较,I/R组和H组再灌注24 h时神经功能缺陷评分和海马神经元凋亡率升高,p-eIf2α表达上调(P〈0.05);与I/R组比较,H组神经功能缺陷评分和海马神经元凋亡率降低,p-eIf2α表达下调(P〈0.05)。结论浅低温通过抑制脑缺血再灌注小鼠海马p-eIF2α表达,减轻内质网应激,抑制神经元凋亡。ObjectiveTo evaluate the effect of mild hypothermia on the expression of phosphorylated eukaryotic translation initiation factor 2α (p-eIf2α) in the hippocampus in a mouse model of cerebral ischemia-reperfusion (I/R).MethodsSixty pathogen-free healthy male C57BL6 mice, aged 8-12 weeks, weighing 20-30 g, were divided into 3 groups (n=20 each) using a random number table: sham operation group (group S), group I/R and mild hypothermia group (group H). Cerebral I/R was induced by 15-min occlusion of bilateral common carotid arteries followed by reperfusion in chloral hydrate-anesthetized mice.Surface cooling was started immediately after reperfusion to maintain the rectal temperature at 32-34 ℃ for 3 h in group H. The neurologic deficit score was evaluated at 24 h of reperfusion.The mice were then sacrificed, brains were immediately removed, and hippocampi were isolated for examination of pathologic changes of hippocampal CA1 region and for determination of neuroapoptosis (by TUNEL) and expression of p-eIf2α (by Western blot). The apoptosis rate was calculated.ResultsCompared with group S, the neurologic deficit scores at 24 h of reperfusion and apoptosis rate of hippocampal neurons were significantly increased, and the expression of p-eIf2α was up-regulated in I/R and H groups (P〈0.05). Compared with group I/R, the neurologic deficit scores at 24 h of reperfusion and apoptosis rate of hippocampal neurons were significantly decreased, and the expression of p-eIf2α was down-regulated in group H (P〈0.05).ConclusionMild hypothermia reduces endoplasmic reticulum stress and inhibits neuroapoptosis through inhibiting the expression of p-eIf2α in the hippocampus in a mouse model of cerebral I/R.
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