目的探讨参芎化瘀胶囊对大鼠全脑缺血再灌注损伤及海马CA1区生长相关蛋白43(growth associated protein 43,GAP43)表达的影响。方法 100只成年SD雄性大鼠随机分为对照组、模型组和参芎化瘀胶囊每日1次组(中药A组),每日2次组(中药B组),每...目的探讨参芎化瘀胶囊对大鼠全脑缺血再灌注损伤及海马CA1区生长相关蛋白43(growth associated protein 43,GAP43)表达的影响。方法 100只成年SD雄性大鼠随机分为对照组、模型组和参芎化瘀胶囊每日1次组(中药A组),每日2次组(中药B组),每日3次组(中药C组),每组20只。采用改良的Pulsinelli四血管闭塞法制备全脑缺血再灌注动物模型。在1、3、7、14天4个时间点通过HE染色观察海马CA1区组织学改变,免疫组织化学法检测海马CA1区GAP43蛋白的表达同时测定行为学评分,第14天通过Western blot法检测海马CA1区GAP43蛋白质含量。结果与对照组比较,模型组各时间点GAP43蛋白表达增高(P<0.05),行为学评分升高(P<0.05),变性神经元增加,存活神经元减少(P<0.05)。与模型组比较,参芎化瘀胶囊各组GAP43蛋白表达均升高(P<0.05),其中中药C组最明显(P<0.01);行为学评分显著降低(P<0.05);变性神经元数量减少,存活神经元数量增加(P<0.05);14天存活神经元数明显增多,其中以中药C组存活神经元数量最多、GAP43蛋白质含量最高,与中药A、B两组比较,差异有统计学意义(P<0.01)。结论参芎化瘀胶囊对大鼠全脑缺血再灌注损伤具有保护作用,其机制可能与升高GAP43的表达有关。展开更多
Background Optic nerve injury, caused by retinal and optic nerve diseases, can eventually result in vision loss. To date, few effective treatments have been discovered to restore visual function. Previous studies show...Background Optic nerve injury, caused by retinal and optic nerve diseases, can eventually result in vision loss. To date, few effective treatments have been discovered to restore visual function. Previous studies showed that recombinant human erythropoietin （rhEPO） has a neuroprotective effect on the central nervous system, particularly in nerve injury. In this study, we investigated the effects of rhEPO on axonal regeneration and functional restoration following optic nerve injury. This was done by measuring the expression of growth associated protein 43 （GAP-43）, a marker for neuronal regeneration, on the retina and flash-visual evoked potential （F-VEP）. Methods Adult Wistar rats were randomly assigned to rhEPO and control （saline） groups. Optic nerve crush injury models were established and rhEPO or saline were immediately injected into the vitreous cavity. The expression of GAP-43 was detected by immunohistochemistry and the F-VEP was measured pre-injury, immediately after injury, 1 week and 2 weeks post-injury. Results No detectable staining for GAP-43 was observed in normal retina. In the control group, the level of GAP-43 expression was higher at 1 week post-injury, but decreased at 2 weeks. In the rhEPO group, the level of GAP-43 expression was notably higher at both 1 week and 2 weeks. At each time point post-injury, the expression of GAP-43 in rhEPO group was significantly higher than the control group （P 〈0.05）. Obvious changes in F-VEP examination were detected immediately after optic nerve injury, including significantly prolonged latency and decreased amplitude of the P1 wave. In the control group, the changes were still obvious at 1 week. The latency was decreased and the amplitude had slightly recovered to 28.23% of the normal value at 2 weeks. In rhEPO group, there was significantly more recovery than the control group at 1 week and 2 weeks post-injury （P 〈0.05）. The latency most close to the normal level and the amplitude had recovered to 65.51% of the normal value at展开更多
文摘Background Optic nerve injury, caused by retinal and optic nerve diseases, can eventually result in vision loss. To date, few effective treatments have been discovered to restore visual function. Previous studies showed that recombinant human erythropoietin （rhEPO） has a neuroprotective effect on the central nervous system, particularly in nerve injury. In this study, we investigated the effects of rhEPO on axonal regeneration and functional restoration following optic nerve injury. This was done by measuring the expression of growth associated protein 43 （GAP-43）, a marker for neuronal regeneration, on the retina and flash-visual evoked potential （F-VEP）. Methods Adult Wistar rats were randomly assigned to rhEPO and control （saline） groups. Optic nerve crush injury models were established and rhEPO or saline were immediately injected into the vitreous cavity. The expression of GAP-43 was detected by immunohistochemistry and the F-VEP was measured pre-injury, immediately after injury, 1 week and 2 weeks post-injury. Results No detectable staining for GAP-43 was observed in normal retina. In the control group, the level of GAP-43 expression was higher at 1 week post-injury, but decreased at 2 weeks. In the rhEPO group, the level of GAP-43 expression was notably higher at both 1 week and 2 weeks. At each time point post-injury, the expression of GAP-43 in rhEPO group was significantly higher than the control group （P 〈0.05）. Obvious changes in F-VEP examination were detected immediately after optic nerve injury, including significantly prolonged latency and decreased amplitude of the P1 wave. In the control group, the changes were still obvious at 1 week. The latency was decreased and the amplitude had slightly recovered to 28.23% of the normal value at 2 weeks. In rhEPO group, there was significantly more recovery than the control group at 1 week and 2 weeks post-injury （P 〈0.05）. The latency most close to the normal level and the amplitude had recovered to 65.51% of the normal value at
