To study the effects of betulin (BE) on myocardial ischemia–reperfusion (I/R) injury in rats, electrocardiogram (ECG) was detected by an electrocardiograph; myocardial infarction was evaluated by triphenyltetrazolium (TTC) staining, serum biochemical indicators myocardial enzymes creatine kinase (CK), lactate dehydrogenase (LDH), aspartate aminotransferase (AST), serum superoxide dismutase (SOD), glutathione (GSH), nitric oxide (NO), and malondialdehyde (MDA); and inflammatory cytokines were tested by using commercial kits. The expression of the Siti1/NLRP3/NF-κB signaling pathway was detected by western blotting and immunohistochemistry experiments. BE improved ECG; reduced myocardial infarction area; decreased CK, LDH, AST, MDA, NO, and inflammatory cytokines; and increased SOD and GSH in I/R rats. In addition, BE also increased Siti1 and decreased the NLRP3/NF-κB signaling pathway in I/R rats. This study shows that the protection of BE is associated with changes in the Siti1/NLRP3/NF-κB pathway.

为了研究桦木脑（BE）对大鼠心肌缺血再灌注（I/R）损伤的影响，通过心电图仪检测心电图（ECG）；心肌梗死评价采用三苯基四唑（TTC）染色、血清生化指标心肌酶、肌酸激酶（CK）、乳酸脱氢酶（LDH）、天冬氨酸转氨酶（AST）、血清超氧化物歧化酶（SOD）、谷胱甘肽（GSH）、一氧化氮（NO） ), 和丙二醛 (MDA); 和炎症细胞因子通过使用商业试剂盒进行测试。通过蛋白质印迹和免疫组织化学实验检测Siti1/NLRP3/NF-κB信号通路的表达。改善心电图；减少心肌梗塞面积；降低 CK、LDH、AST、MDA、NO 和炎性细胞因子；并增加 I/R 大鼠的 SOD 和 GSH。此外，BE 还增加 Siti1 并减少 I/R 大鼠的 NLRP3/NF-κB 信号通路。本研究表明，BE 的保护作用与 Siti1/NLRP3/NF-κB 通路的变化有关。