Background. Coronary heart disease (CHD) is a chronic disease caused by atherosclerosis (AS), which can cause myocardial ischemia, hypoxia, or necrosis, seriously threatening human health. There is an urgent need for effective treatments and drugs to reduce the various risk factors for coronary heart disease and relieve symptoms of angina pectoris and myocardial infarction in patients. Jujuboside A (JuA) is a triterpenoid saponin extracted from jujube seeds, which has various biological activities such as antioxidant, anti-inflammatory, antiapoptotic, and neuroprotective effects. We study the function of JuA in myocardial injury, dyslipidemia, and inflammation in the CHD rat model, to explore its potential mechanism of improving CHD. Methods. A rat model of CHD was established by feeding a high-fat diet. The rats were randomly divided into 5 groups (n = 6): control group, CHD group, JuA 25 mg/kg group, JuA 50 mg/kg group, and JuA 75 mg/kg group. Echocardiography was used to detect the cardiac function parameters of rats in each group, and then, hematoxylin and eosin staining was used to assess the histopathological injury in myocardial tissues. Levels of blood lipids, myocardial injury indexes, and inflammatory factors of rats in each group were measured by biochemical tests and enzyme linked immunosorbent assay, and the levels of Bax, Bcl-2, c-caspase-3, PPAR-α, p65, p-p65, IκBα, and p-IκBα protein expression in myocardial tissues were detected by western blot. Results. Compared with the CHD group, JuA therapy significantly improved injury in myocardial tissue and endothelial tissue. It also strengthened cardiac function, while decreasing total cholesterol, triacylglycerol, and low-density lipoprotein cholesterol levels in the serum and increasing high-density lipoprotein cholesterol levels. In addition, JuA also restrained cardiomyocytes apoptosis and inhibited the inflammatory reaction by reducing TNF-α, IL-1β, and IL-6 expression in myocardial tissues. Furthermore, administration of JuA inhibited the activation of PPAR-α pathway by preventing the phosphorylation of p65 and IκBα in myocardial tissues of CHD rats. Conclusion. JuA may improve cardiac function, alleviate myocardial and endothelial injury, and also ameliorate dyslipidemia and inflammatory reaction in rats with CHD, where JuA probably plays a protective role by inhibiting the activation of PPAR-α pathway.

中文翻译：

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大枣苷 A 通过抑制 PPAR-α 信号通路改善冠心病大鼠心肌细胞凋亡和炎症

背景。冠心病（CHD）是由动脉粥样硬化（AS）引起的慢性疾病，可引起心肌缺血、缺氧或坏死，严重威胁人类健康。迫切需要有效的治疗方法和药物来降低冠心病的各种危险因素，缓解患者心绞痛和心肌梗塞的症状。Jujuboside A (JuA) 是从枣子种子中提取的三萜皂苷，具有抗氧化、抗炎、抗细胞凋亡和神经保护等多种生物活性。我们研究了JuA在CHD大鼠模型心肌损伤、血脂异常和炎症中的作用，探讨其改善CHD的潜在机制。方法。采用高脂饲料喂养建立冠心病大鼠模型。将大鼠随机分为5组（n  =6）：对照组、CHD组、JuA 25 mg/kg组、JuA 50 mg/kg组、JuA 75 mg/kg组。超声心动图检测各组大鼠心功能参数，苏木精伊红染色评估心肌组织病理损伤情况。采用生化检测、酶联免疫吸附法测定各组大鼠的血脂、心肌损伤指标、炎症因子水平,以及Bax、Bcl-2、c-caspase-3、PPAR-α、p65、Western blot检测心肌组织中p -p65、IκBα 、pIκBα蛋白表达量。结果。与CHD组相比，JuA治疗显着改善心肌组织和内皮组织损伤。它还可以增强心脏功能，同时降低血清中的总胆固醇、三酰甘油和低密度脂蛋白胆固醇水平，并增加高密度脂蛋白胆固醇水平。此外，JuA还通过降低心肌组织中TNF- α、IL-1β 、 IL-6的表达，抑制心肌细胞凋亡，抑制炎症反应。此外，JuA的给药通过阻止CHD大鼠心肌组织中p65和IκBα的磷酸化来抑制PPAR-α通路的激活。结论。JuA可以改善CHD大鼠的心功能，减轻心肌和内皮损伤，改善血脂异常和炎症反应，其中JuA可能通过抑制PPAR- α通路的激活而发挥保护作用。