七氟醚预处理对缺血再灌注损伤大鼠的神经保护作用及机制研究

Neuroprotective Effect of Sevoflurane Pretreatment in Rats with Ischemia-reperfusion Injury and Its Possible Mechanism

目的:探讨七氟醚对大鼠缺血再灌注损伤的保护作用。方法:选取48只体重260 g±10 g的健康雄性SD大鼠,随机分为假手术组、损伤组及七氟醚组。假手术组大鼠分离右侧颈总动脉及颈外动脉结扎,不进入颅内置入线栓。损伤组吸入100%纯氧60min之后对右颈内动脉采用尼龙线线栓法制备大脑中动脉阻闭模型(MCAO),七氟醚组吸入2.5%七氟醚(2.5%七氟醚及97.5%氧气)60 min后再行MCAO模型制备。3组大鼠缺血2 h后,进行再灌注24 h。观察三组大鼠的神经功能评分及脑组织TNF-α和IL-1β蛋白水平。结果:假手术组大鼠神经功能评分中位数为18分;损伤组评分中位数为7分;七氟醚组大鼠评分中位数为13分,三组大鼠的评分分布差异具有统计学意义(x2=35.784,P=0.000)。各组大鼠脑组织TNF-α和IL-1β蛋白总体水平差异具有统计学意义(F=15.201,P=0.00;F=26.879,P=0.000)。进一步两两比较后,损伤组TNF-α和IL-1β蛋白水平高于七氟醚组及假手术组,七氟醚组高于假手术组,但远低于损伤组水平,P=0.000。结论:七氟醚对大鼠神经功能有一定保护作用,其机制可能与其影响大鼠脑组织TNF-α及IL-1β蛋白水平,减轻脑缺血再灌注后组织炎症反应有关。

Objective： To explore neuroprotective effect of sevoflurane in rats with ischemia-reperfusion injury. Methods： A total of 48 healthy rats with 260 g± 10 g, were randomly divided into control group, injured group and sevofiurane group. The rats in control group were separated the common carotid artery, and ligatured external carotid artery. The rats in injured group inhaled 100 % pure oxy- gen for 60 min, and MCAO model were performed by using nylon lines bolt in right internal carotid artery. For sevoflurane group, the rats inhaled 2.5 % sevoflurane for 60 min, and MCAO model was performed for them. The TNF-α and IL-1βlevels and neurological score were observed in the three groups. Results： The neurological score in the control group was 18 scores, and was 7 scores in the inju- red group, and was 13 scores in the sevoflurane group. There was significant difference in the scores in the three groups （x2=-35.784, P=0. 000）. There was significant difference in the level of TNF-α and IL-1β in comparison of the three groups （F=1 5.201, P=0.000）（F=26. 879, P=0.000）, The level of TNF-α and IL-1β in injured group was significantly higher than that in control group and sevoflurane group and it was also higher in sevoflurane group than that of control group, P=0,000. Conclusions： Sevoflurane has a certain neuroprotective effect in rats with ischemia-reperfusion injury, which may be associated with decreasing the level of TNF-αand IL-1βin injured brain tis- sues and reducing tissue inflammation afer cerebral ischemia-reperfusion.