摘要
为检查脑撞击伤后 ,脑内自由基含量的变化及中药髓复康对这种变化的调节作用 ,并探讨髓复康脑保护作用的机制 ,将 4 2只清洁级雄性SD大鼠随机分为正常对照 (NG)组、空白对照 (BG)组和髓复康治疗 (SG)组。后 2组行顶骨环钻开窗术后 ,用自由下落的不锈钢重锤造成大脑皮质撞击伤模型。分别在损伤后 6h、3d、7d ,取出损伤区脑组织 ,制备匀浆 ,检测匀浆内超氧化物歧化酶 (SOD)活性和丙二醛 (MDA)的质量摩尔浓度 ,并进行组间比较。发现 :在脑撞击伤 6h后 ,BG和SG组大鼠损伤区脑组织内MDA的质量摩尔浓度和SOD的活性均明显增高 ,组间没有显著性差异 (P >0 .0 5)。脑撞击伤后 3d ,BG组大鼠脑内MDA质量摩尔浓度明显增高 ,SOD活性明显增强 ;而SG组大鼠脑内的MDA增高 ,SOD降低 ,组间差异显著 (P <0 .0 5)。伤后 7d ,BG和SG组大鼠脑内SOD活性恢复到正常水平 ;而SG组大鼠脑内MDA的质量摩尔浓度持续增高 ,组间差异显著 (P <0 .0 5)。结果提示 ,脑撞击伤可以导致脑内自由基的蓄积 。
The objective was to reserch on level change of SOD and MDA after traumatic brai n injur y,and on neuro-protection mechanism of Suifukang(SFK). 42 Sprague-Daleg rat s were divided into three groups: normal control group (NG), blank control group (BG), and SFK group (SG). Cerebral contusion models were prepared by weight dr opping in BG and SG rats. The injury cerebral areas were removed, and homogenize d, on 6th h, 3rd d, and 7th d after the contusion. Levels of SOD and MDA in cere bral ho mog enate were measured. Levels of MDA and SOD were distinctly higher in BG and SG ( P >0.05, between BG and SG) on 6th h after cerebral contusion. Levels of MD A and S OD were distinctly higher in BG than in SG ( P < 0.05) on 3rd d after cere bral contusi on. MDA content was lower in BG than in SG on 7th d after cerebral contusion ( P <0.0 5). The results show that the oxygen free radical increases after cerebra l contusion, the increase is partly inhibited by treatment with SFK.
出处
《首都医科大学学报》
CAS
2004年第1期4-6,共3页
Journal of Capital Medical University
基金
国家自然科学基金(3 0 171189)资助项目