心肌梗死后心肌纤维化是心梗患者发生心源性死亡的重要危险因素之一，我们的既往研究发现补阳还五汤具有防治心梗后心肌纤维化作用。预实验研究发现补阳还五汤能抑制心梗后大鼠心脏转化生长因子β受体1（TGFBR1，调控心肌纤维化关键分子）的表达及其下游信号的激活。我们还采用虚拟筛选技术从补阳还五汤有效成分中筛选出黄芪皂苷IV等20个能与TGFBR1结合的候选化合物，并采用细胞实验初步证实该结果可靠性。据此我们提出以下假说：TGFBR1是补阳还五汤治疗心肌纤维化的潜在靶点，黄芪皂苷IV等候选成分可能是补阳还五汤抑制TGFBR1的物质基础。本项目拟①在动物及细胞水平上激活TGFBR1，验证其在补阳还五汤抗心肌纤维化中的作用；②在细胞模型上筛选候选补阳还五汤中具有抑制TGFBR1作用的有效成分；③采用纳米分子印迹技术去除筛选出的有效成分，以反证这些成分在补阳还五汤调控TGFBR1及抗心肌纤维化中的作用。

Cardiac fibrosis is one of the risk factor heart failure and sudden death after myocardial infarction. In our previous study, we found the resistant effect of Buyang Huaiwu Decoction (BYHWD) on cardiac fibrosis after myocardial infarction. In our preliminary experiment, we found that BYHWD could inhibit TGFBR1, a key receptor of cardiac fibrosis, and the downstream signal activity in rats heart after myocardial infarction. Moreover, we found more than 20 candidate compounds, such as Astragaloside IV, which could bind with TGFBR1 using the molecular docking, and the reliability of this results has been validated in cell experiment. Thus, we put forward the hypothesis that TGFBR1 is the potential treatment target of BYHWD on anti-cardiac fibrosis, 20 candidate compounds may constitute the chemical basis of BYHWD inhibiting TGFBR1. In this study, we will ① consistently activate TGFBR1 to determine whether the role of TGFBR1 in the anti-fibrosis effects of BYHWD in vitro and in vivo; ②verify the effect of candidate compounds on cardiac fibroblasts proliferation and the activation of TGFBR1 pathway; ③knock out the effective candidate compounds from BYHWD using nano-molecular imprinting technique and verify the role of effective candidate compounds on BYHWD inhibiting TGFBR1 and attenuating cardiac fibrosis .