七氟醚预处理对局灶性脑缺血再灌注大鼠T细胞死亡耦联基因8表达的影响

目的：观察七氟醚预处理对局灶性脑缺血再灌注大鼠缺血半暗带内T细胞死亡耦联基因8（TDAG8）表达的影响。方法：选取54只成年雄性SD大鼠，随机分为对照组、再灌注组和七氟醚组，每组18只。采用大脑中动脉内线栓阻断法（middle cerebral artery occlusion，MCAO）制造大鼠局灶性脑缺血再灌注模型。缺血2h后再灌注48h。七氟醚组在造模前吸入最低肺泡有效浓度（MAC）为1的七氟醚30min，对照组和再灌注组则吸入O2。大鼠行神经行为学评分后处死。取大脑行2，3，5-氯化三苯基四氮唑（TFC）染色，计算脑梗死容积百分比，采用蛋白印迹法和RT—PCR法检测脑缺血半暗带内的TDAG8蛋白和mRNA的表达变化。结果：①与对照组相比，再灌注组和七氟醚组脑梗死容积百分比均显著升高（P均〈0．05）；七氟醚组脑梗死容积百分比较再灌注组显著降低（P〈0．05）。②与对照组相比，再灌注组和七氟醚组TDAG8蛋白和mRNA表达均显著升高（P均〈0．05）；七氟醚组较TDAG8的表达再灌注组明显降低（P〈0．05）。结论：七氟醚预处理可降低TDAG8的表达，对脑缺血再灌注损伤具有一定保护作用。

Effect of sevoflurane preconditioning on the expression of T cell death-associated gene 8 following focal cerebral ischemia-reperfusion injury in rats

Objective： To observe the effect of sevoflurane preconditioning on the expression of T cell death-associated gene 8 （TDAGS） in the penumbra of rat cortex after focal cerebral ischemia-reperfusion injury. Methods： Fifty-four adult male SD rats were equally randomly divided into three groups： control group, reperfusion group and sevoflurane group. The focal cerebral isehemia-reperfusion models were established by middle cerebral artery occlusion （MCAO） method. The reperfusion group and sevoflurane group were reperfused for 48 h after isehemia for 2 h. In sevoflurane group the rats inhaled 1 MAC sevoflurane for 30 min before MCAO, while control group and reperfusion group inhaled oxygen. After neurological function appraising, all animals were killed. Infarct volume, as a percentage of volume at normal cerebral hemisphere, was determined by 2, 3, 5-triphenylte-trazolium （TTC） staining and real-time PCR; Western blotting were used to detect the levels of mRNA and protein expression of TDAGS. Results： （1） Compared with the control group, the infarct volume in reperfusion group and sevoflurane group were significantly larger （P 〈 0.05 ） ;compared with the reperfusion group, the infarct volume in sevoflurane group was decreased significantly （P 〈 0.05 ）. （2）Compared with the control group, the expression of mRNA and protein of TDAG8 in reperfusion group and sevoflurane group were increased significantly （ both P 〈 0.05 ） ; the expression of mRNA and protein of TDAG8 in sevoflurane group were markedly decreased than the reperfusion group （P 〈 0.05）. Conclusion： Sevoflurane preconditioning could downregulate the expression of TDAG8 in the penumbra of rat cortex, which might protect against cerebral ischemia from reperfusion insult.