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黄芪丹参配伍提取物经PI3K-AKT信号通路对心肌梗死大鼠的影响 被引量:4

Effect of Compatible Extract of Astragalus and Salvia Miltiorrhiza on Myocardial Infarction Rats via PI3K-AKT Signaling Pathway
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摘要 为观察黄芪丹参配伍提取物对心肌梗死(MI)模型大鼠心肌中磷脂酰肌醇3-激酶(PI3-K)-蛋白质丝氨酸苏氨酸激酶(AKT)信号通路的影响,将8周龄SD雄性大鼠通过“冠状动脉左前降支结扎法”复制成功后,随机分为假手术对照组、模型组、黄芪丹参配伍低、中、高剂量组(10、20、40 mg·kg^-1·d^-1)。对应灌胃给药4周后采用ELISA法、RT-qPCR法和Wstern blot法观察经PI3K-AKT信号通路对MI干预作用。结果表明:黄芪丹参配伍提取物随着浓度增加可明显提高PI3K、AKT表达(P<0.05,P<0.01)。可见黄芪丹参配伍提取物能增强PI3K-AKT信号通路,对保护心肌细胞起到积极作用。 In order to observe the effect of compatible extract of Astragalus and Salvia miltiorrhizaon the phosphatidylinositol 3-kinase (PI3-K)-protein serine threonine kinase (AKT) signaling pathway in myocardial infarction (MI) model rats,the experiment was used to investigate that eight-week-old SD male rats were successfully replicated by “coronary left anterior descending artery ligation”,they were randomly divided into sham-operated control group,model group,low,medium and high dose groups of Astragalus and Salvia miltiorrhiza compatible extract (10,20,40 mg ·kg^-1 ·d ^-1 ). After 4 weeks of intragastric administration,the intervention of MI3 by PI3KAKT signaling pathway was observed by ELISA,RT-qPCR and Wstern blot. The results show that the compatible extract of Astragalus and Salvia miltiorrhiza significantly increased the expression of PI3K and AKT with increasing concentration (P<0.05,P<0.01). It is concluded that the compatible extract of Astragalus andSalviamiltiorrhiza can enhance the PI3K-AKT signaling pathway and play a positive role in protecting cardiomyocytes.
作者 张瓅方 李梦华 ZHANG Li-fang;LI Meng-hua(Henan Key Laboratory of Zhang Zhongjing Formulae and Herbs for Immunoregulation,Nanyang Institute of Technolog 1,Nanyang 473004,China;Nanyang Medical College,Nanyang 473061,China)
出处 《科学技术与工程》 北大核心 2019年第26期113-117,共5页 Science Technology and Engineering
基金 国家自然科学基金(81473438) 河南省高等学校重点科研项目(19A360031,20B360017) 河南省南阳市科技发展计划(KJGG2018077)资助
关键词 黄芪丹参配伍提取物 心肌梗死 PI3K AKT 心肌细胞 Astragalus and Salvia miltiorrhiza compatible extract myocardial infarction PI3K AKT cardiomyocyte
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