中国药理学通报
中國藥理學通報
중국약이학통보
CHINESE PHARMACOLOGICAL BULLETIN
2015年
9期
1239-1243,1244
,共6页
谭实美%韦玲%黄权芳%林兴
譚實美%韋玲%黃權芳%林興
담실미%위령%황권방%림흥
天胡荽%羟基积雪草苷%D-半乳糖%水迷宫%Aβ1 -42 蛋白%Aβ相关基因%突触可塑性
天鬍荽%羥基積雪草苷%D-半乳糖%水迷宮%Aβ1 -42 蛋白%Aβ相關基因%突觸可塑性
천호유%간기적설초감%D-반유당%수미궁%Aβ1 -42 단백%Aβ상관기인%돌촉가소성
hydrocotyle sibthorpioides%madecasso-side%D-galactose%Morris water maze%Aβ1 -42 proteins%Aβ-related genes%synaptic plasticity
目的：探讨天胡荽羟基积雪草苷（madecassoside from hydrocotyle sibthorpioides，MHS）对 D-半乳糖致亚急性衰老模型小鼠学习记忆功能的影响及其作用机制研究。方法SPF 级昆明♂小鼠75只，随机分为正常组、模型组、MHS 低、中、高剂量治疗组。采用 D-半乳糖皮下注射建立亚急性衰老模型，利用 Morris 水迷宫观察小鼠的学习记忆能力；West-ern blot 法测定小鼠海马组织中 Aβ1－42蛋白及突触可塑性相关蛋白的水平；RT-PCR 法检测 Aβ相关基因的表达。结果与模型组比较，MHS 能明显降低 Aβ1－42蛋白的含量（P ＜0.05）；抑制 APP、BACE1和 CatB，同时提高 NEP 和 IDE 的表达（P ＜0.05）；增强突触可塑性相关蛋白 PSD-95、p-NMDAR1、p-CaMKII、p-PKACβ、PKCγ、p-CREB 和 BDNF 的表达（P ＜0.05）。结论MHS 能改善小鼠的学习记忆功能，其机制可能与抑制 Aβ生成与沉积、增强突触可塑性相关蛋白表达有关。
目的：探討天鬍荽羥基積雪草苷（madecassoside from hydrocotyle sibthorpioides，MHS）對 D-半乳糖緻亞急性衰老模型小鼠學習記憶功能的影響及其作用機製研究。方法SPF 級昆明♂小鼠75隻，隨機分為正常組、模型組、MHS 低、中、高劑量治療組。採用 D-半乳糖皮下註射建立亞急性衰老模型，利用 Morris 水迷宮觀察小鼠的學習記憶能力；West-ern blot 法測定小鼠海馬組織中 Aβ1－42蛋白及突觸可塑性相關蛋白的水平；RT-PCR 法檢測 Aβ相關基因的錶達。結果與模型組比較，MHS 能明顯降低 Aβ1－42蛋白的含量（P ＜0.05）；抑製 APP、BACE1和 CatB，同時提高 NEP 和 IDE 的錶達（P ＜0.05）；增彊突觸可塑性相關蛋白 PSD-95、p-NMDAR1、p-CaMKII、p-PKACβ、PKCγ、p-CREB 和 BDNF 的錶達（P ＜0.05）。結論MHS 能改善小鼠的學習記憶功能，其機製可能與抑製 Aβ生成與沉積、增彊突觸可塑性相關蛋白錶達有關。
목적：탐토천호유간기적설초감（madecassoside from hydrocotyle sibthorpioides，MHS）대 D-반유당치아급성쇠로모형소서학습기억공능적영향급기작용궤제연구。방법SPF 급곤명♂소서75지，수궤분위정상조、모형조、MHS 저、중、고제량치료조。채용 D-반유당피하주사건립아급성쇠로모형，이용 Morris 수미궁관찰소서적학습기억능력；West-ern blot 법측정소서해마조직중 Aβ1－42단백급돌촉가소성상관단백적수평；RT-PCR 법검측 Aβ상관기인적표체。결과여모형조비교，MHS 능명현강저 Aβ1－42단백적함량（P ＜0.05）；억제 APP、BACE1화 CatB，동시제고 NEP 화 IDE 적표체（P ＜0.05）；증강돌촉가소성상관단백 PSD-95、p-NMDAR1、p-CaMKII、p-PKACβ、PKCγ、p-CREB 화 BDNF 적표체（P ＜0.05）。결론MHS 능개선소서적학습기억공능，기궤제가능여억제 Aβ생성여침적、증강돌촉가소성상관단백표체유관。
Aim To investigate the protective effect and mechanism of madecassoside from hydrocotyle sibthorpioides (MHS)on learning and memory impair-ment induced by D-galactose (D-gal)in mice.Meth-ods Totally 75 SPF Kunming male mice were divided into normal control group,model group,low-,middle-and high-doses of MHS treated groups.The dementia models were induced with D-gal.The learning and memory functions were tested by Morris water maze, the level of Aβ1 -42 and its related proteins in the hip-pocampus was determined by Western blot,and the ex-pression of Aβ-related genes were determined by RT-PCR.Results Compared with model group,MHS markedly decreased the content of Aβ1 -42 ,inhibited the expression of APP,BACE1 and CatB,but promo-ted the expression of NEP and IDE.In addition,AHS significantly increased the expression of plasticity-relat-ed proteins including PSD-95,p-NMDAR1,p-CaMKII, p-PKACβ,PKCγ,p-CREB and BDNF.Conclusions MHS could remarkably ameliorate the learning and memory impairment induced by D-gal in mice,which may be due to its ability to inhibit the Aβgeneration and deposition and promote synaptic plasticity related protein expression.
