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。
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.
出处
《中国现代医生》
2012年第11期6-7,共2页
China Modern Doctor
关键词
七氟烷后处理
脑
缺血再灌注损伤
凋亡
Sevoflurane postconditioning
Cerebral
Reperfusion injury
Apoptosis
