时珍国医国药
時珍國醫國藥
시진국의국약
LISHIZHEN MEDICINE AND MATERIA MEDICA RESEARCH
2009年
12期
3022-3024
,共3页
丹参酮Ⅱ_A%谷氨酸%γ-氨基丁酸%血管性痴呆
丹參酮Ⅱ_A%穀氨痠%γ-氨基丁痠%血管性癡呆
단삼동Ⅱ_A%곡안산%γ-안기정산%혈관성치태
Tanshinone ⅡA%Glutamate%GABA%Vascular dementia
目的 初步探讨丹参酮主要成分丹参酮II_A对血管性痴呆小鼠的神经保护作用机制.方法 双侧颈总动脉反复缺血/再灌注合并尾部放血降压方法建立血管性痴呆小鼠模型.动物随机分为假手术组、缺血模型组、丹参酮Ⅱ_A低、高剂量(4 mg/kg.d,8 mg/kg.d )治疗组.手术20 d后开始运用Morris水迷宫观测各组的学习记忆功能,然后断头取脑,分离皮层和海马组织,分光光度法测定丙二醛(malondialdehyde, MDA) 含量和超氧化物歧化酶(superoxide dismutase, SOD)以及谷胱甘肽过氧化物酶(GSH-Px)活性的变化;运用高效液相色谱法测定不同组小鼠皮层和海马组织内谷氨酸和γ-氨基丁酸的含量.结果 ①丹参酮Ⅱ_A可以改善血管性痴呆小鼠的学习记忆功能;②丹参酮II_A可减少MDA的生成, 增加SOD、GSH-Px活性;③小鼠手术20 d后,小鼠皮层和海马组织谷氨酸和γ-氨基丁酸的含量减低,丹参酮Ⅱ_A可增加血管性痴呆小鼠皮层和海马组织内谷氨酸和γ-氨基丁酸的含量.结论 丹参酮Ⅱ_A在血管性痴呆小鼠可发挥抗氧化作用并调节兴奋性氨基酸和抑制性氨基酸的含量.
目的 初步探討丹參酮主要成分丹參酮II_A對血管性癡呆小鼠的神經保護作用機製.方法 雙側頸總動脈反複缺血/再灌註閤併尾部放血降壓方法建立血管性癡呆小鼠模型.動物隨機分為假手術組、缺血模型組、丹參酮Ⅱ_A低、高劑量(4 mg/kg.d,8 mg/kg.d )治療組.手術20 d後開始運用Morris水迷宮觀測各組的學習記憶功能,然後斷頭取腦,分離皮層和海馬組織,分光光度法測定丙二醛(malondialdehyde, MDA) 含量和超氧化物歧化酶(superoxide dismutase, SOD)以及穀胱甘肽過氧化物酶(GSH-Px)活性的變化;運用高效液相色譜法測定不同組小鼠皮層和海馬組織內穀氨痠和γ-氨基丁痠的含量.結果 ①丹參酮Ⅱ_A可以改善血管性癡呆小鼠的學習記憶功能;②丹參酮II_A可減少MDA的生成, 增加SOD、GSH-Px活性;③小鼠手術20 d後,小鼠皮層和海馬組織穀氨痠和γ-氨基丁痠的含量減低,丹參酮Ⅱ_A可增加血管性癡呆小鼠皮層和海馬組織內穀氨痠和γ-氨基丁痠的含量.結論 丹參酮Ⅱ_A在血管性癡呆小鼠可髮揮抗氧化作用併調節興奮性氨基痠和抑製性氨基痠的含量.
목적 초보탐토단삼동주요성분단삼동II_A대혈관성치태소서적신경보호작용궤제.방법 쌍측경총동맥반복결혈/재관주합병미부방혈강압방법건립혈관성치태소서모형.동물수궤분위가수술조、결혈모형조、단삼동Ⅱ_A저、고제량(4 mg/kg.d,8 mg/kg.d )치료조.수술20 d후개시운용Morris수미궁관측각조적학습기억공능,연후단두취뇌,분리피층화해마조직,분광광도법측정병이철(malondialdehyde, MDA) 함량화초양화물기화매(superoxide dismutase, SOD)이급곡광감태과양화물매(GSH-Px)활성적변화;운용고효액상색보법측정불동조소서피층화해마조직내곡안산화γ-안기정산적함량.결과 ①단삼동Ⅱ_A가이개선혈관성치태소서적학습기억공능;②단삼동II_A가감소MDA적생성, 증가SOD、GSH-Px활성;③소서수술20 d후,소서피층화해마조직곡안산화γ-안기정산적함량감저,단삼동Ⅱ_A가증가혈관성치태소서피층화해마조직내곡안산화γ-안기정산적함량.결론 단삼동Ⅱ_A재혈관성치태소서가발휘항양화작용병조절흥강성안기산화억제성안기산적함량.
Objective To investigate the underlying neuroprotective mechanisms of Tanshinone ⅡA (TSA) on mouse cerebral ischemia in vivo.Methods Male mice were divided into four groups [sham-operated, ischemic and treated groups (lower dose and higher dose)]. The mice were subjected for ischemia-reperfusion three times on bilateral common carotid arteries by knots to establish models of vascular dementia. After ischemia-reperfusion impairment, TSA (4 mg/kg.d, 8 mg/kg.d) was administered by i.p. for 20 days in treated group. 1. We used morris water maze to investigate the learning and memory;2. Levels of malondialdehyde (MDA), activity of superoxide dismetase (SOD) and glutathione peroxidase (GPX) in brain tissue were detected by spectrophotometer;3. High-performance liquid chromatography(HPLC) with fluorescence detection was applied to measure the contents of glutamate and gamma-aminobutyric acid (GABA) in cortex and hippocampus.Results ①TSA can improve learning and memory deficits in vascular dementia;②An elevation of SOD and GPX activity and decrease of MDA level were shown in TSA treated group after brain ischemia;③Decreased glutamate and gamma-aminobutyric acid induced by chronic brain ischemia were markedly inhibited by TSA pretreatment. Conclusion The neuroprotective effect of TSA are partly due to its functions as follow: anti-free radical injury;regulating the content of glutamate and gamma-aminobutyric acid.
