论文部分内容阅读
目的探讨七氟烷后处理对大鼠脑缺血再灌注Bcl-2和Caspase-3的影响。方法 40只SD雄性大鼠随机分为假手术组(C组)、缺血再灌注组(IP组)、1.0MAC七氟烷后处理组(S1组)和1.5MAC七氟烷后处理组(S2组),每组10只。采用夹闭法制备大鼠颈总动脉缺血模型,缺血20min后再灌注24h。S组于再灌注即刻给予不同浓度七氟烷吸入15min。再灌注24h后断头取脑海马组织,应用免疫组化方法检测Bcl-2和Caspase-3的蛋白表达。结果 IP组Bcl-2的表达较其他组显著减少(P<0.05),Caspase-3的表达较其他组显著增加(P<0.05);S组Bcl-2的表达较其他组显著增加(P<0.05)、Caspase-3的表达较其他组显著减少(P<0.05),且S2组较S1组Bcl-2的表达增加(P<0.05)、Caspase-3的表达减少(P<0.05)。结论七氟烷后处理对大鼠脑缺血再灌注损伤具有一定的保护作用,其作用机制与Bcl-2表达增加、Caspase-3表达减少有关,并呈剂量依赖性。
Objective To investigate the effect of sevoflurane postconditioning on Bcl-2 and Caspase-3 after cerebral ischemia-reperfusion in rats. Methods Forty SD male rats were randomly divided into three groups: sham operation group (C group), ischemia reperfusion group (IP group), 1.0MAC sevoflurane postconditioning group (S1 group) and 1.5MAC sevoflurane postconditioning group S2 group), each group of 10. The model of carotid artery occlusion in rats was made by clipping method. After ischemia for 20min, reperfusion was performed for 24h. S group were given different concentrations of sevoflurane immediately after reperfusion inhalation 15min. After 24 hours of reperfusion, the hippocampus tissues were decapitated and the protein expressions of Bcl-2 and Caspase-3 were detected by immunohistochemistry. Results The expression of Bcl-2 in IP group was significantly lower than that in other groups (P <0.05) and the expression of Caspase-3 was significantly increased (P <0.05). The expression of Bcl-2 in S group was significantly higher than that in other groups (P < 0.05). Caspase-3 expression was significantly decreased (P <0.05) in S2 group compared with S1 group (P <0.05) and Caspase-3 expression was decreased (P <0.05). Conclusion Sevoflurane postconditioning can protect rats from cerebral ischemia-reperfusion injury. The mechanism of action is related to the increase of Bcl-2 expression and the decrease of Caspase-3 expression in a dose-dependent manner.