缺血后处理对大鼠脑缺血再灌注损伤的影响

目的探讨缺血后处理对大鼠脑缺血再灌注损伤的影响。方法成年雄性SD大鼠40只,体质量250～300g,随机分为5组,每组8只,①假手术组(sham组):不施加缺血及再灌注处理;②缺血再灌注1组(I/R1组):给予缺血30min,再灌注24h;③缺血再灌注2组(I/R2组):给予缺血30min,再灌注48h;④缺血后处理1组(Post1组):给予缺血30min,缺血后处理后再灌注24h;⑤缺血后处理2组(Post2组):给予缺血30min,缺血后处理后再灌注48h。用无创动脉夹夹闭双侧颈总动脉实现脑缺血,撤夹实现再灌注。在再灌注即刻给予双侧颈总动脉松夹15s/夹闭15s,如此3次,实现缺血后处理。实验结束制作脑组织匀浆,检测丙二醛(MDA)含量和超氧化物歧化酶(SOD)活性;作石蜡切片,用末端脱氧核苷酸转移酶介导的生物素脱氧尿嘧啶核苷酸缺口末端标记法(TUNEL)观察细胞凋亡情况。结果与sham组相比,I/R1、I/R2、Post1、Post2组MDA含量增高,SOD活性降低(P<0.05);与I/R1组相比,Post1组MDA含量降低,SOD活性升高(P<0.05);与I/R2组相比,Post2组MDA含量降低,SOD活性升高(P<0.05)。sham组可见少量凋亡细胞。与sham组相比,I/R1、I/R2、Post1、Post2组凋亡指数升高(P<0.05);与I/R1组比较,Post1组凋亡指数降低(P<0.05);与I/R2组比较,Post2组凋亡指数降低(P<0.05)。结论缺血后处理可以抑制脑缺血再灌注引起的脂质过氧化反应和细胞凋亡。

Effects of ischemic postconditioning on cerebral ischemic-reperfusion injury in rats

Objective To investigate the effects of ischemic postconditioning on cerebral ischemic-reperfusion injury in rats. Methods Forty mate SD rats （250-300 g in weight） were randomly divided into five groups （n=8 each）： （1） the sham group receiving no ischemia or reperfusion; （2） the ischemic/reperfusion 1 group（I/R1 group） receiving 30rain ischemia and 24 h reperfusion; （3） the ischemic/reperfusion 2 group（I/R2 group）receiving 30 min ischemia and 48 h reperfusion; （4） postconditiouing 1 group （Postl group） receiving 30 rain ischemia and 24 h reperfusion with post- conditioning; （5） postconditioning 2 group （Post2 group） receiving 30 min ischemia and 48 h reperfusion with postcon- ditioning. Ischemia was achieved by clipping of bilateral common carotid arteries, reperfusion by withdrawal of the clips, and postconditioning by 15 s clipping and 15 s unclipping of the bilateral common carotid arteries for three cycles immediately at the time of reperfusion. At the end of the experiment, all of the rats were killed. Brain tissue homogenate were collected in order to measure the contents of MDA and the activity of SOD. Paraffin-embedded brain sections were prepared for study of cell apoptosis by TUNEL method. Results Compared with the sham group, the I/R1, I/R2, Post1, and Post2 groups showed increased MDA contents and reduced SOD activities （P〈0.05）. Increased MDA contents and reduced SOD activities were also shown in Postl group vs I/R1 group （P〈0.05）, and in Post2 group vs I/R2 group （P〈0.05）. Cell apoptosis was modest in the sham group. In contrast, I/R1, I/R2, Postl and Post2 groups showed higher level of apoptosis （P〈0.05）. Lower apoptosis index was found in Postl group vs I/R1 group （P〈0.05）, and in Post2 group vs I/R2 group （P〈0.05）. Conclusion Postconditioning could inhibit lipid peroxidation and brain cell apoptosis induced by ischemic/reperfusion.