CAJ | 학술논문

目的：探讨染料木黄酮（ GEN）对全脑缺血（ GCI）大鼠海马CA1区神经元的神经保护作用及其可能的机制。方法建立大鼠4动脉结扎全脑缺血模型，实验动物随机分为假手术组（ sham）、缺血再灌注组（ I/R）、GEN处理组、ICI 182，780组和溶剂对照组。采用Fluoro-Jade B和神经元特异性核蛋白（ NeuN）染色观察海马CA1区神经元存活情况，TUNEL技术观察海马CA1区神经元的凋亡。 Morris水迷宫观察大鼠的空间学习和记忆功能。结果 GEN发挥神经保护作用的最佳剂量为1．0 mg/kg；与sham组相比，I/R组和溶剂对照组海马CA1区TUNEL阳性神经元数量显著增多（ P＜0．01），而1．0 mg/kg GEN可显著降低缺血后TUNEL阳性神经元数量（ P＜0．01）；与I/R组相比，GEN能明显改善缺血后大鼠的空间学习和记忆能力。缺血前侧脑室给予ICI 182，780可显著降低GEN的神经保护作用（P＜0．01）。结论低剂量（1．0mg/kg） GEN可显著降低缺血后大鼠海马CA1区神经元损伤，改善认知功能，其分子机制可能与雌激素受体活性密切相关。
목적：탐토염료목황동（ GEN）대전뇌결혈（ GCI）대서해마CA1구신경원적신경보호작용급기가능적궤제。방법건립대서4동맥결찰전뇌결혈모형，실험동물수궤분위가수술조（ sham）、결혈재관주조（ I/R）、GEN처리조、ICI 182，780조화용제대조조。채용Fluoro-Jade B화신경원특이성핵단백（ NeuN）염색관찰해마CA1구신경원존활정황，TUNEL기술관찰해마CA1구신경원적조망。 Morris수미궁관찰대서적공간학습화기억공능。결과 GEN발휘신경보호작용적최가제량위1．0 mg/kg；여sham조상비，I/R조화용제대조조해마CA1구TUNEL양성신경원수량현저증다（ P＜0．01），이1．0 mg/kg GEN가현저강저결혈후TUNEL양성신경원수량（ P＜0．01）；여I/R조상비，GEN능명현개선결혈후대서적공간학습화기억능력。결혈전측뇌실급여ICI 182，780가현저강저GEN적신경보호작용（P＜0．01）。결론저제량（1．0mg/kg） GEN가현저강저결혈후대서해마CA1구신경원손상，개선인지공능，기분자궤제가능여자격소수체활성밀절상관。
Objective To explore the neuroprotective role of Genistein (GEN) on hippocampal CA1 neurons and the possible mechanism following global cerebral ischemia ( GCI) in rats.Methods Seventy five rats were subjected to global cerebral ischemia ( GCI ) by four-vessel occlusion and randomly divided into five groups , sham, ischemia/reperfusion (I/R), GEN, ICI 182,780 and vehicle groups.Fluoro-Jade B and neuron-specific nuclear-binding protein ( NeuN) staining was used to observe CA 1 neuronal survival .TUNEL was used to detect apoptotic neurons .Spatial learning and memory function of the rats were evaluated by Morris water maze .Results The best dose of neuroprotective role of GEN was 1.0mg/kg body weight.Compared with sham, TUNEL-positive neurons in the hippocampal CA1 region increased significantly in I/R and vehicle groups (P<0.01), while post-treatment with GEN (1.0mg/kg) at 5min after ischemia by tail vein injection decreased markedly (P<0.01).Treatment of 1.0mg/kg GEN markedly attenuated spatial learning and memory deficits of the rats after ischemic insult compared to I /R group.Furthermore, ICI 182,780 significantly abolished the neuroprotective role of GEN (P <0.01).Conclusion The low-dose (1.0mg/kg) GEN significantly attenuates neuronal damage and cognitive deficits following GCI in rats , and the mechanism may be involved in estrogen receptor activity.