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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Effective delivery of Pep-1-cargo protein into ischemic neurons and long-term neuroprotection of Pep-1-SOD1 against ischemic injury in the gerbil hippocampus.
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Effective delivery of Pep-1-cargo protein into ischemic neurons and long-term neuroprotection of Pep-1-SOD1 against ischemic injury in the gerbil hippocampus.

机译：有效地将Pep-1-货物蛋白递送到缺血神经元中，并对Pep-1-SOD1进行长期的神经保护，以防止沙鼠海马的缺血性损伤。

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We examined the intracellular delivery of Pep-1-cargo protein against transient ischemic damage in the hippocampal CA1 region in gerbils. For this study, we introduced green fluorescent protein (GFP) and constructed Pep-1-GFP protein. At 12h after Pep-1-GFP treatment, GFP fluorescence was shown in almost CA1 pyramidal neurons in ischemic animals; in the sham-operated group, GFP fluorescence was shown in a few pyramidal neurons. Next, we confirmed the long-term effects of Pep-1-Cu,Zn-superoxide dismutase 1 (SOD1) against ischemic damage. In behavioral test, locomotor activity was significantly increased in Pep-1- and Pep-1-SOD1-treated groups 1 day after ischemia/reperfusion; the locomotor activity in the Pep-1-treated group was higher than that of the Pep-1-SOD1-treated group. Thereafter, the locomotor activity in both groups was decreased with time. Four days after ischemia/reperfusion, the locomotor activity in the Pep-1-SOD1-treated group was similar to that of the sham group; in the Pep-1-treated group, the activity was lower than that of the sham group. In the histochemical study, the cresyl violet positive neurons in the Pep-1-SOD1-treated group were abundantly detected in the hippocampal CA1 region 5 days after ischemia/reperfusion. In biochemical study, SOD1 protein level and activity in all Pep-1-treated ischemic groups were significantly lower than that of the Pep-1-SOD1-treated group. Our results indicate that Pep-1-cargo fusion proteins can be efficiently delivered into neurons in the ischemic hippocampus, and that Pep-1-SOD1 treatment in ischemic animals show a neuroprotection in the ischemic hippocampus for a long time.
机译：我们检查了Pep-1-货物蛋白的细胞内传递对沙土鼠海​​马CA1区的短暂性脑缺血损伤的作用。对于本研究，我们引入了绿色荧光蛋白（GFP）并构建了Pep-1-GFP蛋白。 Pep-1-GFP处理后12h，在缺血动物的几乎CA1锥体神经元中显示GFP荧光。在假手术组中，在一些锥体神经元中显示了GFP荧光。接下来，我们证实了Pep-1-Cu，Zn超氧化物歧化酶1（SOD1）对缺血性损伤的长期作用。在行为测试中，缺血/再灌注1天后，Pep-1和Pep-1-SOD1处理组的运动活动显着增加。 Pep-1治疗组的自发活动高于Pep-1-SOD1治疗组。此后，两组的运动活性均随时间降低。缺血/再灌注后四天，Pep-1-SOD1治疗组的运动活动与假手术组相似;在Pep-1治疗组中，活性低于假手术组。在组织化学研究中，在缺血/再灌注后5天，在Pep-1-SOD1治疗组中的甲酚紫阳性神经元在海马CA1区大量检出。在生化研究中，所有Pep-1处理的缺血组的SOD1蛋白水平和活性均明显低于Pep-1-SOD1处理的组。我们的结果表明，Pep-1货物融合蛋白可以有效地递送到缺血海马的神经元中，并且在缺血动物中Pep-1-SOD1处理在缺血海马中显示了长期的神经保护作用。

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