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首页> 外文期刊>International Journal of Neuroscience >Neuroprotective effect of L-arginine in a neonatal rat model of hypoxic-ischemia
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Neuroprotective effect of L-arginine in a neonatal rat model of hypoxic-ischemia

机译:L-精氨酸在缺氧缺血新生大鼠模型中L-精氨酸的神经保护作用

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Aim: The aim of the present study is to investigate the neuroprotective effects of L-Arginine (L-arg) in the seven-day-old rat hypoxia-ischemia model. Materials and methods: L-Arginine (n = 10) or saline (n = 8) was administered intraperitoneally to seven-day-old rats before hypoxia-ischemia. In addition, 18 seven-day-old rats were given l-Arginine (n = 10) or saline (n = 8) after hypoxic-ischemic insult. Neuronal apoptosis was investigated by terminal dUDP-biotin nick end-labeling (TUNEL) following three days of recovery. The ratios of right side numerical density to the sum of right and left sides’ numerical densities (right apoptosis index) were calculated for every brain region in rats receiving L-arginine and they were compared with the vehicle groups. Results: Right side apoptosis indexes of the hippocampus (mean±SD; 35.0±16.1) and striatum (41.9±16.0) were significantly decreased in the L-Arginine post-treatment groups when compared to vehicles (61.0 ± 17.0 and 62.4 ±27.0 respectively) (p < 0.05). There was no significant difference in the right apoptosis indexes of the cortex between L-Arginine post-treated group and the vehicle group. There were also no significant differences between the right side apoptosis indexes of the L-Arginine pretreatment groups and those of the vehicle group in any of the three regions (p > 0.05). Conclusions: It is concluded that neuronal apoptosis due to hypoxic-ischemic injury may likely to be reduced by post-treatment of L-Arginine in the neonatal rat model and L-Arginine provides a new possibility for neuroprotective strategies based on NO production.
机译:目的:本研究的目的是探讨L-精氨酸(L-Arg)在七天血液大鼠缺氧缺血模型中的神经保护作用。材料和方法:L-精氨酸(n = 10)或盐水(n = 8)在缺氧缺血前腹膜内腹膜施用至七天大鼠。此外,在缺氧缺血性侮辱后,给出18只七天历史大鼠L-精氨酸(n = 10)或盐水(n = 8)。在恢复三天后,通过末端DUDP-BIOTIN缺口末端标记(TUNEL)研究了神经元细胞凋亡。针对接受L-精氨酸的大鼠中的每种大脑区域计算右侧数值密度对右侧和左侧左侧凋亡指数的总和的比率,并与载体组进行比较。结果:与车辆(61.0±17.0和62.4±27.4±27.4±27.4±27.4±27.0,L-精氨酸后处理组(平均±SD; 35.0±16.1)和纹状体(41.9±16.0)的右侧凋亡指标(平均值±SD; 35.0±16.0)显着降低)(p <0.05)。 L-精氨酸后治疗后组和载体组皮质的右凋亡指数没有显着差异。 L-精氨酸预处理基团的右侧凋亡指数与三个区域中任一方的右侧凋亡指数和载体组的右侧凋亡指标之间也没有显着差异(P> 0.05)。结论:得出结论是,由于新生大鼠模型中L-精氨酸的后处理,缺氧缺血性损伤引起的神经元细胞凋亡可能降低,L-精氨酸为基于没有生产的神经保护策略提供了新的可能性。

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