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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 ,服用髓复康可以在一定程度上抑制脑撞击伤诱发的自由基增高
To examine the changes of free radical content in the brain and the regulatory effect of the Chinese medicine Puyeukang on brain damage after brain injury, and to explore the mechanism of the protective effect of phelilcotol, 42 male clean SD rats were randomly assigned to The normal control (NG) group, the blank control (BG) group, and the spiracrolone treatment (SG) group. The posterior two groups of patients underwent the drilling of the coronoid ring to open the window, and a free-falling stainless steel weight was used to create a cerebral cortex impact injury model. At 6h, 3d, and 7d after injury, the injured brain tissue was removed to prepare a homogenate. Superoxide dismutase (SOD) activity and malondialdehyde (MDA) molarity were measured and compared between groups. . It was found that the concentration of MDA and the activity of SOD in the injured brain tissue of the BG and SG groups were significantly increased 6 h after brain injury. There was no significant difference between the groups (P > 0.05). After 3d of brain impact injury, the concentration of MDA in the brain of BG rats was significantly increased and the SOD activity was significantly increased. However, the MDA in the brain of rats in SG group was increased and the SOD was decreased. There was a significant difference between groups (P < 0.05). . At 7 days after injury, the activity of SOD in the brains of rats in BG and SG groups returned to normal levels, while the MDA concentration in brains of rats in SG group continued to increase, with significant differences between groups (P < 0.05). The results suggest that brain impact injury can lead to the accumulation of free radicals in the brain. Taking Pycnoxycan can inhibit the increase of free radicals induced by brain impact injury to some extent.