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背景:黄芪在机体免疫功能调节中具有重要作用,而在对急性颅脑损伤干预中是否具有神经元保护作用,且其发挥作用的途径何在?目的:观察黄芪对脑损伤后脑组织一氧化氮合酶活性的影响。设计:随机对照的实验。单位:兰州军区神经外科研究所。对象:实验于2001-09/12在兰州军区神经外科研究所实验室完成。取健康雄性SD大鼠54只,随机分为3组:脑损伤组(n=24),黄芪组(n=24),对照组(n=6),损伤组与黄芪组均分为伤后0.5,2,6和24h4个时间点,每个时间点6只动物。方法:脑损伤组和黄芪组制备脑损伤模型,对照组仅开骨窗,不致伤。黄芪组致伤后立即腹腔注射黄芪200mg/kg,用化学定量法检测大鼠脑损伤后不同时间点脑组织中一氧化氮合酶的活性。主要观察指标:各组大鼠脑组织中一氧化氮合酶活性。结果:54只大鼠全部进入结果分析。脑损伤组、黄芪组大鼠在伤后0.5h一氧化氮合酶活性较对照组升高[46.44±13.45)(43.15±12.43),(40.46±12.85)nkat/L,P<0.05],伤后2h达高峰[(67.49±22.45),(64.26±19.78)nkat/L,P<0.01],伤后6h开始下降[(63.46±24.68),(52.91±21.36)nkat/L,P<0.01],伤后24h降至基础水平[(41.23±12.57),(40.92±12.25)nkat/L,P>0.05]。黄芪组在伤后2,6h一氧化氮合酶活性较损伤组明显降低(P<0.01,0.05)。结论:颅脑损伤后,受损脑组织中一氧化氮合酶活性呈节段性升高,黄芪可通过抑制损伤后脑组织中一氧化氮合酶活性,起到保护创伤神经元的作用。
Background: Astragalus plays an important role in the regulation of immune function in the body, but whether it has a neuroprotective effect in the intervention of acute brain injury, and its role in the path? Purpose: To observe the effect of astragalus on brain tissue nitric oxide after brain injury The effect of enzyme activity. Design: Randomized controlled experiments. Unit: Lanzhou Military Region Institute of Neurosurgery. Subject: The experiment was performed at the Laboratory of Neurosurgery Institute of Lanzhou Military Region from September to December 2001. Fifty healthy male SD rats were randomly divided into 3 groups: brain injury group (n=24), astragalus group (n=24) and control group (n=6). Injury group and astragalus group were divided into two groups after injury. 0.5, 2, 6 and 24h 4 time points, 6 animals per time point. METHODS: The brain injury model was prepared in the brain injury group and the Huangqi group. The control group only opened the bone window without injury. Intraperitoneal injection of Scutellariae Radix Astragali was 200 mg/kg immediately after injury in the Astragalus membranaceus group. The activity of nitric oxide synthase in brain tissue at different time points after brain injury was determined by chemical quantification. MAIN OUTCOME MEASURES: Activity of nitric oxide synthase in brain tissue of each group. Results: All 54 rats entered the results analysis. Nitric oxide synthase activity in the brain injury group and the Huangqi group was higher than that in the control group at 0.5h after injury (46.44±13.45) (43.15±12.43), (40.46±12.85) nkat/L, P<0.05]. The peak value was reached after 2h [(67.49±22.45), (64.26±19.78) nkat/L, P<0.01], and it began to decline after 6h [(63.46±24.68), (52.91±21.36) nkat/L, P<0.01] , It decreased to basal level 24 hours after injury [(41.23±12.57), (40.92±12.25) nkat/L, P>0.05]. The activity of nitric oxide synthase in the Astragalus group at 2 and 6 hours after injury was significantly lower than that in the injury group (P<0.01, 0.05). Conclusion: After craniocerebral injury, the activity of nitric oxide synthase in damaged brain tissue is increased in segments. Huangqi can protect the injured neurons by inhibiting the activity of nitric oxide synthase in brain tissue after injury.