本研究旨在调查奇力强心胶囊（QL）在丙酸脱氧皮质酮盐（DOCA）诱导的保留射血分数（HFpEF）大鼠心力衰竭模型中的保护效应和作用机制。对非肾切除的60只斯普拉格·道利（SD）大鼠进行了DOCA盐注射，并在饮水中加入1％的盐水进行4周，并随机分为四组：模型组（n = 15），Sac / Val组（Sacubitril Valsartan 0.02 g / kg，n = 15），QL-L组（奇力强心胶囊0.25 g / kg，n = 15）和QL-H组（Qiliqiangxin 1 g / kg，n = 15）。另设有正常组（n = 15）。测量血压、N-末端脑钠肽前体（NT-proBNP）、心脏指数、超声心动图和血液动力学来评估心脏功能。进行混杂和小麦胚凝集素（WGA）染色以观察纤维化沉积和心肌细胞的横截面积（CSA）。通过ELISA检测血清细胞因子的浓度水平，包括肿瘤坏死因子-α（TNF-α），白细胞介素（IL）-2，IL-6和IL-10炎症因子；通过Western-blot检测基质金属蛋白酶2（MMP2），基质金属蛋白酶9（MMP9），转化生长因子-β1（TGF-β1），核因子-κB（NF-κB），Smad同源物2（Smad2）和Smad同源物3（Smad3）的表达。与模型组相比，QL治疗明显改善了DOCA盐诱导的HFpEF大鼠心脏功能，显示出心脏指数的降低，EF和E / A比率的增加，左室前/后壁（LVAW / LVPW）的减少，等容舒张期时间（IVRT）的时间收缩，-dP / dt Max，Tau的减少以及血清NT-ProBNP的降低。混杂和WGA染色表明，与模型组相比，QL抑制了纤维化沉积和心肌肥大，这与降低TGF-β1，MMP2，MMP9，Smad2和Smad3等心脏重塑蛋白的表达水平一致。此外，QL治疗抑制了心脏组织中NF-κB的表达，降低了血清促炎细胞因子TNF-α和IL-2的浓度，而增加了IL-10的浓度。QL通过改善舒张功能，防止左室肥厚和改善DOCA盐诱导的HFpEF模型中的炎症反应，改善了DOCA盐诱导的HFpEF大鼠心脏功能并抑制了心肌纤维化。

The aim of this study was to investigate the protective effect and mechanism of action (MOA) of Qiliqiangxin capsule (QL) in the deoxycorticosterone acetate (DOCA) salt-induced rat heart failure with preserved ejection fraction (HFpEF) model.Nono-nephrectomy sixty Sprague Dawley (SD) rats received DOCA salt injection and 1% saline in drinking water for 4 weeks and were randomly divided into four groups on average: Model group (n=15), Sac/Val group (Sacubitril Valsartan 0.02 g/kg, n=15), QL-L group (Qiliqiangxin 0.25 g/kg, n=15) and QL-H group (Qiliqiangxin 1 g/kg, n=15). Another Normal group was set (n=15). Blood pressure, N-terminal pro-brain natriuretic peptide (NT-proBNP), cardiac index, echocardiography, and hemodynamics were measured to evaluate heart function. Masson and Wheat germ agglutinin (WGA) staining was performed to observe the fibrosis deposition and the cross-sectional area (CSA) of cardiomyocytes. The concentration levels of the serum cytokines, including tumor necrosis factor-α (TNF-α), interleukin (IL)-2, IL-6, and IL-10 inflammatory factors, were detected by ELISA; matrix metalloproteinase 2 (MMP2), matrix metalloproteinase 9 (MMP9), transforming growth factor-β1 (TGF-β1), nuclear factor-κB (NF-κB), Smad homologue 2 (Smad2) and Smad homologue 3 (Smad3) expression were detected by Western-blot.Compared with the Model group, QL treatment significantly ameliorated the heart function in DOCA salt-induced rat HFpEF model, showing a decrease in cardiac index, an increase of the EF and E/A ratio, a reduction in the left ventricular anterior/posterior wall (LVAW/LVPW), in the time contraction of isovolumic diastolic time (IVRT), -dP/dt Max, and Tau, and the decrease of serum NT-ProBNP. Masson and WGA staining indicated that QL inhibited the fibrosis deposition and the myocardial hypertrophy compared with the Model group, which was consistent in reducing the protein expression levels of cardiac remodeling such as TGF-β1, MMP2, MMP9, Smad2, and Smad3. Moreover, QL treatment inhibited the expression of NF-κB in the heart tissues and decreased the serum concentration of pro-inflammatory cytokines TNF-α and IL-2, instead, increasing the IL-10 concentration.QL improved the cardiac function and inhibited the myocardial fibrosis in DOCA salt-induced rat HFpEF by improving diastolic dysfunction, preventing left ventricular hypertrophy, and ameliorating the inflammatory responses model in DOCA salt-induced rat HFpEF model.