世界中医药
世界中醫藥
세계중의약
WORLD CHINESE MEDICINE
2015年
4期
560-563
,共4页
人参总皂苷%右室肥厚%细胞外信号调节激酶%丝裂素活化蛋白激酶磷酸酶 -1
人參總皂苷%右室肥厚%細胞外信號調節激酶%絲裂素活化蛋白激酶燐痠酶 -1
인삼총조감%우실비후%세포외신호조절격매%사렬소활화단백격매린산매 -1
Total ginsenosides%Right ventricular hypertrophy%Extracellular-regulated kinase%Mitogen-activated protein kinase phosphatase-1
目的：观察人参总皂苷（Total Ginsenosides，TG）对野百合碱（Monocrotaline，MCT）所致大鼠右心室肥厚的影响并探讨其与细胞外信号调节激酶（ERK）信号通路的关系。方法：雄性 SD 大鼠随机分为正常对照组，MCT 模型组，TG 20 mg／（kg·d）、40 mg／（kg·d）、60 mg／（kg·d）剂量组，各组动物均给药18 d。测定各组大鼠的右室肥厚指数（RVHI）、右心重／体重（RVW／BW）；透射电镜观察心肌细胞超微结构的改变；Real time RT －PCR 检测心肌组织 ERK1mRNA 的表达，West-ern blotting 检测心肌组 MKP －1蛋白质的表达。结果：TG 预防给药均使 RVHI、RV ／BW 表达明显降低，改善超微结构损伤，降低心肌组织 ERK1mRNA 和提高 MKP －1蛋白质的表达。结论：TG 能明显改善 MCT 诱导的大鼠右心室肥厚，其抗心肌肥厚作用至少与抑制 ERK1信号转导通路有关。
目的：觀察人參總皂苷（Total Ginsenosides，TG）對野百閤堿（Monocrotaline，MCT）所緻大鼠右心室肥厚的影響併探討其與細胞外信號調節激酶（ERK）信號通路的關繫。方法：雄性 SD 大鼠隨機分為正常對照組，MCT 模型組，TG 20 mg／（kg·d）、40 mg／（kg·d）、60 mg／（kg·d）劑量組，各組動物均給藥18 d。測定各組大鼠的右室肥厚指數（RVHI）、右心重／體重（RVW／BW）；透射電鏡觀察心肌細胞超微結構的改變；Real time RT －PCR 檢測心肌組織 ERK1mRNA 的錶達，West-ern blotting 檢測心肌組 MKP －1蛋白質的錶達。結果：TG 預防給藥均使 RVHI、RV ／BW 錶達明顯降低，改善超微結構損傷，降低心肌組織 ERK1mRNA 和提高 MKP －1蛋白質的錶達。結論：TG 能明顯改善 MCT 誘導的大鼠右心室肥厚，其抗心肌肥厚作用至少與抑製 ERK1信號轉導通路有關。
목적：관찰인삼총조감（Total Ginsenosides，TG）대야백합감（Monocrotaline，MCT）소치대서우심실비후적영향병탐토기여세포외신호조절격매（ERK）신호통로적관계。방법：웅성 SD 대서수궤분위정상대조조，MCT 모형조，TG 20 mg／（kg·d）、40 mg／（kg·d）、60 mg／（kg·d）제량조，각조동물균급약18 d。측정각조대서적우실비후지수（RVHI）、우심중／체중（RVW／BW）；투사전경관찰심기세포초미결구적개변；Real time RT －PCR 검측심기조직 ERK1mRNA 적표체，West-ern blotting 검측심기조 MKP －1단백질적표체。결과：TG 예방급약균사 RVHI、RV ／BW 표체명현강저，개선초미결구손상，강저심기조직 ERK1mRNA 화제고 MKP －1단백질적표체。결론：TG 능명현개선 MCT 유도적대서우심실비후，기항심기비후작용지소여억제 ERK1신호전도통로유관。
Objective:To investigate the inhibition of total ginsenosides (TG)on right ventricular hypertrophy induced by mono-crotaline(MCT)and explore the effects of TG on extracellular-regulated kinase(ERK)signal transduction in rat.Methods:Male Sprague Dawley rats were randomly divided into the normal group,MCT group and 20 mg/(kg·d),40 mg/(kg·d),60 mg/(kg ·d)dose TG treatment group.Ventricular hypertrophy index(RVHI)was measured by the weight ratio of RV to left ventricle plus septum,and by observing the ultrastructural changes of myocardial cell with transmission electron microscope.The ERK1 mRNA and mitogen-activated protein kinase phosphatase-1(MKP-1)protein expression of right ventricle tissue were detected by real-time RT-PCR,Western blotting.Results:TG treatment could significantly reduce RVHI,RVW/BW.The swollen and misshapen mito-chondria could be improved by TG.TG also could down-regulate ERK1 mRNA expression and enhance MKP-1 protein expression. Conclusion:TG could significantly attenuate MCT-induced cardiac hypertrophy in rat by suppressing ERK Signaling pathway.
