首页> 外文期刊>Biological & pharmaceutical bulletin >Berberry Extract Reduces Neuronal Damage and N-Methyl-D-aspartate Receptor 1 Immunoreactivity in the Gerbil Hippocampus after Transient Forebrain Ischemia
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Berberry Extract Reduces Neuronal Damage and N-Methyl-D-aspartate Receptor 1 Immunoreactivity in the Gerbil Hippocampus after Transient Forebrain Ischemia

机译:小berry提取物减少短暂性前脑缺血后沙鼠海马中的神经元损伤和N-甲基-D-天冬氨酸受体1免疫反应性。

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摘要

In the present study,we studied the neuroproteetive effects of berberry extract (BE) against ischemic damage and the temporal and spatial alterations of N-methyl-D-aspartate receptor type 1 (NR1) and NR2A/2B immunoreactivities in the gerbil hippocampal CA1 region after transient ischemia to examine anti-ischemic effects and its role in transient forebrain ischemia.In the vehicle-treated group,the percentage of cresyl violet positive pyramidal cells in the CA1 region was about 11.4% compared to the sham-operated group 4d after ischemic insult.BE showed neuroproteetive effects against ischemic damage after ischemia-reperfusion.In the BE-treated groups,about 60-75% of CA1 pyramidal cells were stained with cresyl violet 4 d after ischemic insult.We observed the percentage of berberine (7.45+0.85 mg/g in BE) by HPLC,which is active ingredient of BE.NR1 immunoreactivity in the stratum pyramidale of the CA1 region in the vehicle-treated group was significantly increased at 30min after transient forebrain ischemia,while at this time the NR1 immunoreactivity in the BE-treated groups was significantly low compared to the vehicle-treated group.The pattern of NR2A/B immunoreactivity in the stratum pyramidale of the BE-treated group and its protein levels were similar to that in the vehicle-treated group after ischemic insult.These results suggest that BE has potent neuroproteetive effects against ischemic damage via the reduction of NR1 activity.
机译:在本研究中,我们研究了小berry提取物(BE)对缺血损伤以及沙鼠海马CA1区N-甲基-D-天门冬氨酸受体1型(NR1)和NR2A / 2B免疫反应性的时空变化短暂缺血后观察其抗缺血作用及其在短暂前脑缺血中的作用。在媒介物治疗组中,缺血后4d,假手术组的CA1区甲酚紫阳性锥体细胞百分比约为假手术组在缺血再灌注后,BE对缺血性损伤具有神经保护作用。在BE治疗组中,缺血后4 d约60-75%的CA1锥体细胞被甲酚紫染色。我们观察到小碱的百分比(7.45+高效液相色谱法(HPLC)测得的浓度为0.85 mg / g(BE),在转染后30分钟,赋形剂治疗组CA1区域锥体层的BE.NR1免疫反应性显着增加nt前脑缺血,但此时BE治疗组的NR1免疫反应性显着低于媒介物治疗组.BE治疗组的锥体层中NR2A / B免疫反应的模式及其蛋白水平分别为这些结果表明,BE通过降低NR1活性对缺血性损伤具有有效的神经保护作用。

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