黄芪对急性脑损伤后一氧化氮合酶活性的抑制作用

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±1285)nkat/L,P＜0.05],伤后2 h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24 h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.

Influence of astragalus membranaceous in inhibiting the activity of nitric oxide synthase after acute brain injury

BACKGROUND: Astragalus membranaceus plays an important role in the adjustment of immunological function. Whether does it have protective effect on neuron in the intervention of acute craniocerebral injury and what is the pathway in effect?OBJECTIVE: To observe the effect of astragalus membranaceus on activity of nitric oxide synthetase after brain injury.DEDIGN: Randomized controlled trial.SETTING: Neurosurgery institute of Lanzhou Military Area Command of Chinese PLA.MATERIALS: This experiment was completed in the Laboratory of Neurosurgery Institute of Lanzhou Military Area Command of Chinese PLA. Fifty-four healthy SD rats were divided randomly into 3 groups: brain injury group( n=24), astragalus membranaceus group( n = 24) and control group( n = 6). Injury and astragalus membranaceus groups were sampled at 4different time points(0.5 hour, 2 hours, 6 hours, and 24 hours) after injury,6 rats were sacrificed at each time point.METHODS: The brain injury and astragalus membranaceus groups were prepared by improved Feeney' s free falling method. Bone windows were opened for the control group, but no brain injury produced. After injury, rats in astragalus membranaceus group were immediately injected 200 mg/kg astragalus membranaceus intraperitoneally rat cerebral injury models were established and the nitric oxide synthetase concentration was tested at different time points.MAIN OUTCOME MEASURES: Activity of nitric oxide synthetase in the brain tissue of rats in each group.RESULTS: All 54 rats entered the final analysis. Nitric oxide synthetase activity in brain injury and astragalus membranaceus groups increased sharply contrasting with control group at 30 minute after injury [ (46.44 ± 13.45),(43.15 ± 12.43), (40. 46 ± 12. 85) nkat/L, P ＜0.05], reaching the peak at 2hours[ (67.49 ± 22.45), (64. 26 ± 19.78) nkat/L, P ＜ 0.01 ], starting to drop from6 hours [(63.46±24. 68), (52.91 ±21.36) nkat/L, P ＜0. 01], and getting to basic level at 24 hours[ (41.23 ± 12. 57), (40.92 ± 12. 25) nkat/L,P ＞ 0.05 ]. In the astragalus membranaceus treated group, nitric oxide synthetase activity dropped at 2 hours and 6 hours after injury contrasting with injury group( P ＜ 0. 05, P ＜ 0. 01 respectively).CONCLUSION: Nitric oxide synthetase activity increases in the injured brain tissue and astragalus membranaceus can protect injured neuron by inhibiting nitric oxide synthetase activity.