20(S)-protopanaxadiol (PPD) is an active natural product which is transformed from protopanaxadiol-type ginsenosides. The present study was conducted to evaluate the effects of PPD on myocardial ischemia/reperfusion (I/R) injury in a rat model. PPD (20mg/kg) or positive-control drug Diltiazem (10mg/kg) was administered daily for 7 days before left anterior descending I/R operation. After 2-hour reperfusion, changes of cardiac morphology, structure, and function were evaluated by HE staining and echocardiography. Myocardial infarct size was assessed using nitroblue tetrazolium staining. The activities of cardiac enzymes in serum were also evaluated. Cardiomyocyte apoptosis was detected using the terminal dUTP nick end labelling (TUNEL) assay. The extent of oxidative stress was evaluated according to the activities of superoxide dismutase (SOD) and glutathione per oxidase (GPx) and the levels of malondialdehyde (MDA). Western blot and immunohistochemistry were used to determine the expression of apoptosis associated proteins, including Bcl-2, Bax, cleaved Caspase-3, cleaved Caspase-9, and cytochrome C. According to the results, PPD reduced I/R‑induced increases in myocardial infarct size and improved cardiac function. Furthermore, PPD decreased cardiomyocyte apoptosis on TUNEL staining, which was verified by increased Bcl-2, and decreased expression of Bax, cytochrome C, cleaved Caspase-9, and cleaved Caspase-3 in I/R rat myocardium. Additionally, PPD reduced MDA levels and increased the anti-oxidative capacity by upregulating the activities of SOD and GPx. Taken together, the results suggest that PPD serves a protective role against oxidative stress and cardiomyocyte apoptosis during myocardial ischemia/reperfusion injury.

20(S)-protopanaxadiol (PPD) 是一种活性天然产物，由原人参二醇型人参皂苷转化而来。本研究旨在评估 PPD 对大鼠模型心肌缺血/再灌注 (I/R) 损伤的影响。在左前降支 I/R 手术前每天给药 PPD（20mg/kg）或阳性对照药物地尔硫卓（10mg/kg），持续 7 天。再灌注2小时后，通过HE染色和超声心动图评估心脏形态、结构和功能的变化。使用硝基四氮唑染色评估心肌梗塞大小。还评估了血清中心肌酶的活性。使用末端 dUTP 缺口末端标记 (TUNEL) 测定法检测心肌细胞凋亡。根据超氧化物歧化酶 (SOD) 和谷胱甘肽过氧化酶 (GPx) 的活性和丙二醛 (MDA) 的水平评估氧化应激的程度。使用蛋白质印迹和免疫组织化学确定凋亡相关蛋白的表达，包括 Bcl-2、Bax、cleaved Caspase-3、cleaved Caspase-9 和细胞色素 C。根据结果，PPD 减少了 I/R 诱导的增加心肌梗死面积和心脏功能改善。此外，PPD 降低了 TUNEL 染色中的心肌细胞凋亡，这通过增加的 Bcl-2 得到证实，并降低了 I/R 大鼠心肌中 Bax、细胞色素 C、裂解的 Caspase-9 和裂解的 Caspase-3 的表达。此外，PPD 通过上调 SOD 和 GPx 的活性降低 MDA 水平并增加抗氧化能力。综合起来，