基于组效关系和Ca2+-CaN-NFAT3信号通路研究益心泰有效组分抗心衰的作用机制

Heart failure is a cardiac dysfunction syndrome which results from various heart diseases, such as dilated cardiomyopathy, hypertension and myocardial infarction. Myocardial remodeling is the basic pathophysiological mechanism of heart failure. The Ca2+-CaN-NFAT3-mediating signaling pathway has been regarded as the main pathological cardiac hypertrophy signaling pathway at present. Previous studies have shown that Yi-xin-tai exerts anti-heart failure effect through regulating the Ca2+-CaN-NFAT3-mediating signaling pathway. The rabbit model of heart failure caused by by DCM,hypertension and cardiac myocardial infartion of Xin-qi deficiency complicated blood stasis and edema syndrome and myocardial fibrosis model are used in our study,which may display the advantage of treating different diseases with the same therapeutic principle. Based on Composition-Activity Relationship and Ca2+-CaN-NFAT3-mediating signaling pathway, we try to deeply explore the anti-heart failure mechanisms of active components of Yi-xin-tai from multiple points of view and different level, which can eventually provide scientific evidence for its comprehensive effects in diagnosis and treatment based on an overall analysis of the illness and the patient's condition.

心力衰竭是各种心脏疾病导致心功能不全的一种临床综合征，常见的病因有扩张型心肌病、高血压、心肌梗死。心肌重构是心力衰竭发生的基本病理生理机制。Ca2+-CaN-NFAT3信号通路是体内最主要的病理性心肌肥厚信号通路。前期研究表明，益心泰可通过抑制Ca2+-CaN-NFAT3信号通路抗心衰。本课题拟采用扩张型心肌病、高血压、心肌梗死三种不同原发病心力衰竭心气虚血瘀水停证模型兔以及心肌成纤维细胞作为体外研究对象，体现“异病同治”的辨证施治优势，并基于组效关系和Ca2+-CaN-NFAT3通路，从整体角度多层次深入探讨益心泰有效成分抗心衰的作用机制，为其辨证施治之综合效应提供依据。

心力衰竭是各种心脏疾病导致心功能不全的一种临床综合征，常见的病因有扩张型心肌病、高血压、心肌梗死。心肌重构是心力衰竭发生的基本病理生理机制。Ca2+-CaN-NFAT3通路是体内最主要的病理性心肌肥厚信号通路。前期研究表明，益心泰可通过抑制Ca2+-CaN-NFAT3信号通路抗心衰。本课题采用扩张型心肌病、高血压、心肌梗死三种不同原发病心力衰竭心气虚血瘀水停证模型兔以及心肌成纤维细胞作为体外研究对象，观察益心泰有效组分对兔血清ANP,BNP、心脏超声等心功能指标,心肌细胞内Ca2+浓度,心肌组织CaN活性,心肌组织CaN、NFAT3 蛋白及其mRNA表达等指标的影响，基于组效关系和Ca2+-CaN-NFAT3通路，从整体角度多层次深入探讨益心泰有效成分抗心衰的作用机制，为其辨证施治之综合效应提供依据。