七氟烷后处理对大鼠脑缺血再灌注损伤PI3K/Akt通道的影响 |
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引用本文: | 李婧,韩冲芳,任倩倩,王鑫,闫晓笑.七氟烷后处理对大鼠脑缺血再灌注损伤PI3K/Akt通道的影响[J].中国现代医生,2012,50(11):6-7. |
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作者姓名: | 李婧 韩冲芳 任倩倩 王鑫 闫晓笑 |
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作者单位: | 1. 山西医科大学麻醉学系,山西太原,030001 2. 山西医科大学麻醉学系,山西太原 030001;山西医科大学附属山西大医院麻醉科,山西太原 030032 |
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摘 要: | 目的探讨七氟烷后处理对大鼠脑缺血再灌注损伤PI3K/Akt通道的影响。方法 SD雄性大鼠40只随机分为5组(n=8):假手术对照组(C组)、缺血再灌注损伤组(IR组)、2.5%七氟烷后处理组(S组)、2.5%七氟烷+磷脂酰肌醇-3激酶/蛋白激酶B抑制剂LY294002组(S+LY组)和溶剂对照组(DMSO组)。采用双侧颈总动脉阻断联合低血压法制备脑缺血再灌注模型。于再灌注结束后处死大鼠取海马,光镜下观察海马病理学变化,采用免疫组化法检测Caspase-3及p-Akt的表达,TUNEL法检测细胞凋亡。结果与C组相比,其余4组AI、Caspase-3及p-Akt表达均增加(P〈0.05)。与IR组相比,S组AI及Caspase-3表达显著降低(P〈0.05),p-Akt表达明显增加(P〈0.05),S+LY组及DMSO组各指标表达无明显差异(P〉0.05)。结论七氟烷后处理可能通过激活PI3K/Akt通道,抑制Caspase-3表达,减少大鼠脑缺血再灌注损伤时神经元细胞凋亡,发挥脑保护作用。
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关 键 词: | 七氟烷后处理 脑 缺血再灌注损伤 凋亡 |
Effect of sevoflurane postcondionting on PI3K/Akt after cerebral ischemia-reperfusion in rats |
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Authors: | LI Jing HAN Chongfang REN Qianqian WANG Xin YAN Xiaoxiao |
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Institution: | 1.Department of Anesthesiology,Shanxi Medical University,Taiyuan 030001,China;2.Department of Anesthesiology,Af-filiated Shanxi Great Hospital of Shanxi Medical University,Taiyuan 030032,China |
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Abstract: | Objective To investigate the effect of sevoflurane postconditioning on PI3K/Akt after cerebral ischemia-reperfu-sion in rats.Methods Forty male SD rats were randomly assigned to five groups(with 8 rats each): C group,ischemi-a-reperfusion(IR group),2.5% sevoflurane postconditioning group(S group),2.5% sevoflurane+LY294002 group(S+LY group) and DMSO group.The global cerebral ischemia/reperfusion(I/R) was induced by bilateral common cephalic artery occlusion and maintained 20min combined with hypotension.We observed the morphological changes of hippocampal neu-rons by HE.Expression of Caspase-3 and p-Akt were observed by immunohistochemical method.To examine the apoptotic pyramidal neuron by TUNEL test.Results Compared with C group,the apoptotic rate,Caspase-3 expression and p-Akt expression were significantly increased in other four groups(P < 0.05).Compared with IR group,the apoptotic rate and Caspase-3 expression were significantly decreased,p-Akt expression was significantly increased in S group(P < 0.05).There was no significant difference in all variables among IR group,S+LY group and DMSO group(P > 0.05).Conclusion Sevoflurane postcondnioning can protect brain IR injury in rat by decreasing the expression of Caspase-3 and this anti-apoptotic effect may be achieved by activation of PI3K/Akt signaling pathway. |
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Keywords: | Sevoflurane postconditioning Cerebral Reperfusion injury Apoptosis |
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