CAJ | 학술논문

目的：探讨α-硫辛酸( ALA)对血管性痴呆( VD)大鼠的神经保护作用及机制。方法40只健康成年雄性Wistar大鼠行双侧颈总动脉结扎以制备血管性痴呆大鼠模型。动物随机分为假手术组、血管性痴呆组、α-硫辛酸50 mg/( kg·d)干预血管性痴呆组( VD+ALA)和α-硫辛酸50 mg/( kg·d)干预假手术组( sham+ALA)。利用Morris水迷宫观测各组动物学习记忆能力,流式细胞仪测定各组动物脑组织线粒体膜电位( mitochondrial membrane potential,MMP)、活性氧自由基( reactive oxygen species,ROS)的水平,脑组织超氧化物歧化酶( superoxide dismutase, SOD)含量。结果与假手术组相比,血管性痴呆大鼠脑组织中MMP下降,ROS含量升高,SOD含量下降；α-硫辛酸干预血管性痴呆组与血管性痴呆组相比大鼠学习记忆能力改善,脑组织MMP明显升高,ROS明显下降,SOD含量增加。结论线粒体功能障碍和氧化应激损伤在VD发病中有非常重要的作用,ALA能够保护脑线粒体功能,减轻氧化应激损伤,改善认知功能。
목적：탐토α-류신산( ALA)대혈관성치태( VD)대서적신경보호작용급궤제。방법40지건강성년웅성Wistar대서행쌍측경총동맥결찰이제비혈관성치태대서모형。동물수궤분위가수술조、혈관성치태조、α-류신산50 mg/( kg·d)간예혈관성치태조( VD+ALA)화α-류신산50 mg/( kg·d)간예가수술조( sham+ALA)。이용Morris수미궁관측각조동물학습기억능력,류식세포의측정각조동물뇌조직선립체막전위( mitochondrial membrane potential,MMP)、활성양자유기( reactive oxygen species,ROS)적수평,뇌조직초양화물기화매( superoxide dismutase, SOD)함량。결과여가수술조상비,혈관성치태대서뇌조직중MMP하강,ROS함량승고,SOD함량하강；α-류신산간예혈관성치태조여혈관성치태조상비대서학습기억능력개선,뇌조직MMP명현승고,ROS명현하강,SOD함량증가。결론선립체공능장애화양화응격손상재VD발병중유비상중요적작용,ALA능구보호뇌선립체공능,감경양화응격손상,개선인지공능。
Objective To explore the neuroprotective effects and mechanisms of alpha-lipoic acid( ALA) in a rat model of vascular de-mentia( VD) . Methods Bilateral common carotid arteries occlusion( BCCAO) was applied in adult male Wistar rats to establish VD model. Animals were randomly assigned into four groups:sham( sham-operated) group,VD group,VD+ALA group,sham+ALA group. The model rats were intraperitoneally injected with normal saline in VD group,and 50 mg/kg alpha-lipoic acid in VD+ALA group. The sham-operated rats were intraperitoneally injected with 50 mg/kg alpha-lipoic acid in sham+ALA group. Learning and memory deficits were tested by Morris water maze. Flow cytometry was applied to detect mitochondrial membrane potential and the level of reactive oxy-gen species( ROS) in brain tissues. Spectrophotometry was used to determine the concentrations of superoxide dismutase( SOD) in brain tissues. Results In brains of the VD rats,mitochondrial membrane potential significantly decreased,ROS significantly increased,and SOD significantly decreased. However,ALA significantly improved cognitive deficits,protected mitochondrial membrane potential,signif-icantly decreased ROS and increased superoxide dismutase. Conclusion Mitochondrial damage and oxidative stress play important roles in the pathogenesis of vascular dementia. ALA could protect the mitochondrial function,ameliorate the oxidative damage and im-prove the cognitive function.