Chen D M, Li W H, Xu B X, Tao X B, Chen J
Department of Natural and Synthetic Drug Research, College of Pharmacy, Second Military Medical University, Shanghai, China.
Zhongguo Yao Li Xue Bao. 1994 Sep;15(5):469-72.
Brain injury in Mongolian gerbil (Merisones unguiculatus) was induced by occluding bilateral common carotid arteries for 60 min followed by reperfusion for 5 or 30 min. Oxygen free radicals in brain tissue were measured by electron spin resonance (ESR) technique, malondialdehyde (MDA) was measured by fluorescence spectrometry, and superoxide dismutase (SOD) was measured by nitrite kit. Oxygen free radicals and MDA were not significantly increased, but activities of T-SOD and Mn-SOD were decreased after 60 min of cerebral ischemia. The free radicals were increased at 5-min reperfusion, and then reduced to the level of ischemia group after 30-min reperfusion. MDA was increased remarkably after reperfusion of 30 min, whereas the activity of SOD continued to decrease. Sodium diethyldithiocarbamate (DTC), i.v. 5-100 mg.kg-1 15 min before occlusion, decreased the production of MDA and increased the activities of T-SOD and Mn-SOD. The formation of oxygen free radicals was depressed by i.v. DTC 50 mg.kg-1. The result suggested that the protective effects of DTC on ischemia-reperfusion-induced brain injury might be induced by scavenging the oxygen free radicals, increasing the Mn-SOD activity and decreasing the production of MDA.
通过阻断双侧颈总动脉60分钟，随后再灌注5或30分钟，诱导长爪沙鼠（Merisones unguiculatus）脑损伤。采用电子自旋共振（ESR）技术测定脑组织中的氧自由基，用荧光光谱法测定丙二醛（MDA），用亚硝酸盐试剂盒测定超氧化物歧化酶（SOD）。脑缺血60分钟后，氧自由基和MDA没有显著增加，但总超氧化物歧化酶（T-SOD）和锰超氧化物歧化酶（Mn-SOD）的活性降低。再灌注5分钟时自由基增加，再灌注30分钟后降至缺血组水平。再灌注30分钟后MDA显著增加，而SOD活性持续下降。在阻断前15分钟静脉注射二乙基二硫代氨基甲酸钠（DTC）5-100mg·kg-1，可降低MDA的产生，增加T-SOD和Mn-SOD的活性。静脉注射50mg·kg-1的DTC可抑制氧自由基的形成。结果表明，DTC对缺血再灌注诱导的脑损伤的保护作用可能是通过清除氧自由基、增加Mn-SOD活性和减少MDA的产生来实现的。
