Myocardial ischemia/reperfusion injury（MIRI）会导致心肌组织坏死，增加心肌梗死大小。该研究调查了冠心丹参方（GXDSF）对大鼠MIRI的保护作用和机制。在大鼠中进行了MIRI模拟实验；用缺氧重氧法建立了H9C2心肌细胞损伤模型。GXDSF 可显著减少心肌缺血面积， 减少心肌结构损伤，降低血清中白细胞介素（IL-1β、IL-6）的水平，降低心肌酶活性，增加超氧化物歧化酶（SOD）活性，减少大鼠MIRI病例中的谷胱甘肽。GXDSF还可以减少心肌组织细胞中核苷酸结合寡聚化结构域富含亮氨酸重复和脉络膜域包含的NLRP3、IL-1β、caspase-1和gasDermin D（GSDMD）的表达。丹参酚B和三七皂苷R1可保护H9C2心肌细胞免受缺氧/重氧损伤，降低细胞上清物中肿瘤坏死因子α（TNF-α）和IL-6的水平，降低H9C2心肌细胞中NLRP3、IL-18、IL-1β、caspase-1和GSDMD的表达。GXDSF可以减少大鼠MIRI中的心肌梗死面积，减轻心肌结构损伤，这可能与调节NLRP3有关。GXDSF可以通过降低炎症因子和控制局部细胞死亡信号通路来减少大鼠心肌梗死损伤的MIRI，改善心肌缺血损伤中的结构性损害，并降低心肌组织炎症和氧化应激。

Myocardial ischemia/reperfusion injury (MIRI) leads to myocardial tissue necrosis, which will increase the size of myocardial infarction. The study examined the protective effect and mechanism of the Guanxin Danshen formula (GXDSF) on MIRI in rats.MIRI model was performed in rats; rat H9C2 cardiomyocytes were hypoxia-reoxygenated to establish a cell injury model.The GXDSF significantly reduced myocardial ischemia area, reduced myocardial structural injury, decreased the levels of interleukin (IL-1β, IL-6) in serum, decreased the activity of myocardial enzymes, increased the activity of superoxide dismutase (SOD), and reduced glutathione in rats with MIRI. The GXDSF can reduce the expression of nucleotide- binding oligomerization domain, leucine-rich repeat and pyrin domain containing nod-like receptor family protein 3 (NLRP3), IL-1β, caspase-1, and gasdermin D (GSDMD) in myocardial tissue cells. Salvianolic acid B and notoginsenoside R1 protected H9C2 cardiomyocytes from hypoxia and reoxygenation injury and reduced the levels of tumor necrosis factor α (TNF-α) and IL-6 in the cell supernatant, decreasing the NLRP3, IL-18, IL-1β, caspase-1, and GSDMD expression in H9C2 cardiomyocytes. GXDSF can reduce the myocardial infarction area and alleviate the damage to myocardial structure in rats with MIRI, which may be related to the regulation of the NLRP3.GXDSF reduces MIRI in rat myocardial infarction injury, improves structural damage in myocardial ischemia injury, and reduces myocardial tissue inflammation and oxidative stress by lowering inflammatory factors and controlling focal cell death signaling pathways.