Song Wen-ying, Dong Hai-long, Cheng Qiong, Lu Zhi-hong, Wang Hui, Meng Jing-ru, Xiong Li-ze
Department of Anesthesiology, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, China.
Zhonghua Yi Xue Za Zhi. 2008 Aug 26;88(33):2355-9.
To test the hypothesis that spinal cord protection induced by ischemic postconditioning is mediated by an increase of endogenous antioxidant enzyme activities during reperfusion phase in spinal cord.
Seventy-eight male New Zealand rabbits were randomly divided into 3 groups: Sham group (n = 18) undergoing sham operation without aortic occlusion; ischemia/reperfusion (I/R) group (n = 30) undergoing occlusion of the infrarenal abdominal aorta for 20 min, followed by reperfusion; and postconditioning (PostC) group (n = 30) undergoing occlusion of the infrarenal abdominal aorta for 20 min followed by 3 cycles of 30 s reperfusion/30 s ischemia just at the onset of reperfusion. 30 min, and 1, 3, 6, 24, and 48 h after reperfusion 5 rabbits from each group (and 3 from the Sham group) were killed with their spinal cords taken out, and spectrophotometric method was used to determine the antioxidant enzyme activity and malondialdehyde (MDA) content 6, 24, and 48 h after reperfusion motor function scoring of the hind limbs was conducted.
(1) The motor function scores of the PostC group were significantly higher than those of the I/R group 6, 24, and 48 h after reperfusion (all P < 0.05). (2) The activities of superoxide dismutase (SOD) and catalase (CAT) in the spinal cord tissue of the PostC group 30 min-6 h after reperfusion were all significantly higher than those of the I/R group (all P < 0.05). There were no significant differences in the activity of glutathione peroxidase (GSH-px) at different time points between the PostC and I/R groups. (3) The MDA levels 24 h and 48 h after reperfusion of the PostC group were both significantly lower than that of the I/R group (both P < 0.01).
Ischemic postconditioning shows effect against spinal cord ischemic-reperfusion injury mediated, at least partially, by up-regulating the activities of SOD and CAT in spinal cord during early reperfusion phase.
验证脊髓缺血后处理诱导的脊髓保护作用是通过再灌注期内源性抗氧化酶活性增加介导的这一假说。
78只雄性新西兰兔随机分为3组：假手术组（n = 18），行假手术，不阻断主动脉；缺血/再灌注（I/R）组（n = 30），阻断肾下腹主动脉20分钟，随后再灌注；后处理（PostC）组（n = 30），阻断肾下腹主动脉20分钟，在再灌注开始时进行3个周期的30秒再灌注/30秒缺血。再灌注后30分钟、1、3、6、24和48小时，每组处死5只兔子（假手术组处死3只），取出脊髓，采用分光光度法测定再灌注后6、24和48小时抗氧化酶活性及丙二醛（MDA）含量，并对后肢进行运动功能评分。
（1）再灌注后6、24和48小时，PostC组的运动功能评分显著高于I/R组（均P < 0.05）。（2）再灌注后30分钟至6小时，PostC组脊髓组织中超氧化物歧化酶（SOD）和过氧化氢酶（CAT）活性均显著高于I/R组（均P < 0.05）。PostC组和I/R组在不同时间点的谷胱甘肽过氧化物酶（GSH-px）活性无显著差异。（3）PostC组再灌注后24小时和48小时的MDA水平均显著低于I/R组（均P < 0.01）。
缺血后处理对脊髓缺血-再灌注损伤具有保护作用，至少部分是通过在再灌注早期上调脊髓中SOD和CAT的活性介导的。
