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基于钙调磷酸酶-活化T细胞核因子3信号转导通路探究 四逆汤治疗心力衰竭的分子机制
引用本文:党万太,苗维纳,杨晓放,童妍. 基于钙调磷酸酶-活化T细胞核因子3信号转导通路探究 四逆汤治疗心力衰竭的分子机制[J]. 中国实验方剂学杂志, 2011, 17(22): 201-204
作者姓名:党万太  苗维纳  杨晓放  童妍
作者单位:成都中医药大学基础医学院,成都,610075
摘    要:目的:分析钙调磷酸酶-活化T细胞核因子3(CaN-NFAT3)信号转导通路在四逆汤治疗心衰过程中的分子机制。方法:取SPF级SD大鼠60只,分10只作为空白对照组外,余50只采用连续ip盐酸阿霉素(0.002 5 g.kg-1,每周1次,连续6周)方法复制大鼠心力衰竭模型,待造模成功后将动物分为模型对照组与四逆汤高、中、低剂量(5.6,2.8,1.4 g.kg-1)治疗组,用四逆汤水煎液治疗8 d后,分别检测CaN的活性、心肌钙含量、去磷酸化NFATc蛋白的相对表达。结果:四逆汤水煎液高、中剂量治疗组CaN活性均明显低于模型组(P<0.01)、钙含量明显升高(P<0.01)、大鼠心肌组织中去磷酸化NFATc/β-actin吸光度比值较模型对照组显著降低(P<0.01)。结论:CaN-NFAT3信号转导通路的抑制为四逆汤治疗心力衰竭的关键分子机制。

关 键 词:钙调磷酸酶-活化T细胞核因子3  四逆汤  心衰  分子机制
收稿时间:2011-03-24

Based on CaN-NFAT3 Signalling Pathways to Explore the Molecular Mechanism of Sini Decoction in Treatments of Heart Failure
DANG Wan-tai,MIAO Wei-n,YANG Xiao-fang and TONG Yan. Based on CaN-NFAT3 Signalling Pathways to Explore the Molecular Mechanism of Sini Decoction in Treatments of Heart Failure[J]. China Journal of Experimental Traditional Medical Formulae, 2011, 17(22): 201-204
Authors:DANG Wan-tai  MIAO Wei-n  YANG Xiao-fang  TONG Yan
Affiliation:School of Basic Medicine, Chengdu University of Traditional Chinese Medicine, Chengdu 610075, China;School of Basic Medicine, Chengdu University of Traditional Chinese Medicine, Chengdu 610075, China;School of Basic Medicine, Chengdu University of Traditional Chinese Medicine, Chengdu 610075, China;School of Basic Medicine, Chengdu University of Traditional Chinese Medicine, Chengdu 610075, China
Abstract:Objective:To analysis the molecular mechacnism of the signal transduction Calcineurin-nuclear factor of activated T cells(CaN-NFAT3) in the treatment of heart failure with Sini decoction.Method:Sixty SPF grade SD rats were dividied into control group(n=10)and model group(n=50).Adriamycin was given intraperitoneally to fifty to copy the model of heart failure.The heart failure rats were divided into model group and Sini decoction treating group(high,middle and low dose group).Giving Sini decoction to the tre...
Keywords:CaN-NFAT3  Sini decoction  congestive heart failure  molecular mechanism
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