CAJ | 학술논문

目的：探讨丹皮酚对血管性认知障碍（VCI）小鼠认知功能及海马神经元损伤的影响。方法：雄性C57BL/6小鼠60只，随机分为假手术（Sham）组、模型（VCI）组、丹皮酚（Pae）低、中、高剂量治疗组，每组12只。采用双侧颈总动脉结扎（2VO）制备小鼠反复缺血再灌注VCI模型，Morris水迷宫检测小鼠的认知功能，尼氏染色观察小鼠海马神经元的形态学变化，比色法检测海马SOD活性、MDA和NO含量的变化。结果：VCI小鼠认知功能下降（P＜0.01），海马CA1区神经元变性坏死，MDA和NO含量增加，SOD活性降低（P＜0.01）；丹皮酚中、高剂量治疗可显著提高VCI小鼠的学习记忆能力，减少VCI所致的海马CA1区神经元死亡，并降低MDA和NO含量，升高SOD活性（P＜0.05或P＜0.01）。结论：丹皮酚可有效增强VCI小鼠的认知功能，并改善海马神经元病理改变，可能与其抗氧化应激有关。
목적：탐토단피분대혈관성인지장애（VCI）소서인지공능급해마신경원손상적영향。방법：웅성C57BL/6소서60지，수궤분위가수술（Sham）조、모형（VCI）조、단피분（Pae）저、중、고제량치료조，매조12지。채용쌍측경총동맥결찰（2VO）제비소서반복결혈재관주VCI모형，Morris수미궁검측소서적인지공능，니씨염색관찰소서해마신경원적형태학변화，비색법검측해마SOD활성、MDA화NO함량적변화。결과：VCI소서인지공능하강（P＜0.01），해마CA1구신경원변성배사，MDA화NO함량증가，SOD활성강저（P＜0.01）；단피분중、고제량치료가현저제고VCI소서적학습기억능력，감소VCI소치적해마CA1구신경원사망，병강저MDA화NO함량，승고SOD활성（P＜0.05혹P＜0.01）。결론：단피분가유효증강VCI소서적인지공능，병개선해마신경원병리개변，가능여기항양화응격유관。
Objective: To investigate the effects of paeonol on cognitive dysfunctions and hippocampal neuronal injury of vascular cognitive impairment (VCI) mice.Methods: Sixty C57BL/6 mice were randomly di-vided into sham opertated group, the VCI group and the paeonol treated groups (low, medium and high dose). The VCI models were dupilicated by the bilateral common carotid artery occlusion (2VO). The cognitive impairments were observed by Morris water maze. The contents of MDA, SOD and NO in hippocampus were determined spectrometrically. The hippocampal neuron injuries in the CA1 region were detected by nissle staining.Results:VCI induced the decreased cognitive function and neuron injury in the hippocampal CA1 region (P<0.01). And MDA and NO contents were signiifcantly increased, whereas SOD activity was dramatically decreased after VCI (P<0.01). Compared with VCI model goup, the medium and high dose of paeonol treatment signiifcantly im-proved cognitive impairments and reduced pathological changes in hippocampal CA1 region (P<0.05,P<0.01). In additon, the medium and high dose of paeonol treatment markedly improved SOD activity, decreased MDA and NO contents in hippocampus (P<0.05,P<0.01).Conclusion: Paeonol can improve cognitive impairments and neuronal injury in VCI mice, which may be related to the increased antioxidative ability of brain tissue.