Sleep deprivation (SD) may lead to serious myocardial injury in cardiovascular diseases. Saponins extracted from the roots of Panax notoginseng, a traditional Chinese medicine beneficial to blood circulation and hemostasis, are the main bioactive components exerting cardiovascular protection in the treatment of heart disorders, such as arrhythmia, ischemia and reperfusion injury, and cardiac hypertrophy. This study aimed to explore the protective effect of stem-leaf saponins from Panax notoginseng (SLSP) on myocardial injury in SD mice. SD was induced by a modified multi-platform method. Cardiac morphological changes were assessed by hematoxylin and eosin (H&E) staining. Heart rate and ejection fraction were detected by specific instruments. Serum levels of atrial natriuretic peptide (ANP) and lactate dehydrogenase (LDH) were measured with biochemical kits. Transmission electron microscopy (TEM), immunofluorescent, and Western blotting analysis were used to observe the process and pathway of autophagy and apoptosis in heart tissue of SD mice. In vitro, rat H9c2 cells pretreated with rapamycin and the effect of SLSP were explored by acridine orange staining, transient transfection, flow cytometry, and Western blotting analysis. SLSP prevented myocardial injury, such as morphological damage, accumulation of autophagosomes in heart tissue, abnormal high heart rate, serum ANP, and serum LDH induced by SD. In addition, it reversed the expressions of proteins involved in the autophagy and apoptosis and activated PI3K/Akt/mTOR signaling pathway that is disturbed by SD. On H9c2 cells induced by rapamycin, SLSP could markedly resume the abnormal autophagy and apoptosis. Collectively, SLSP attenuated excessive autophagy and apoptosis in myocardial cells in heart tissue induced by SD, which might be acted through activating PI3K/Akt/mTOR signaling pathway.

睡眠剥夺 (SD) 可能导致心血管疾病中的严重心肌损伤。从根部提取的皂苷三七是一种活血止血的中药，是治疗心律失常、缺血再灌注损伤、心肌肥厚等心脏疾病中发挥心血管保护作用的主要生物活性成分。本研究旨在探讨茎叶皂苷的保护作用。三七(SLSP) 对 SD 小鼠心肌损伤的影响。SD是通过改进的多平台方法诱导的。通过苏木精和伊红 (H&E) 染色评估心脏形态学变化。通过特定仪器检测心率和射血分数。用生化试剂盒测量心房利钠肽（ANP）和乳酸脱氢酶（LDH）的血清水平。采用透射电镜(TEM)、免疫荧光和Western blotting分析观察SD小鼠心脏组织自噬和凋亡的过程和途径。体外,通过吖啶橙染色、瞬时转染、流式细胞术和Western blotting分析,探讨了雷帕霉素预处理大鼠H9c2细胞及SLSP的作用。SLSP可预防心肌损伤，如SD诱导的形态学损伤、自噬体在心脏组织中的积累、异常高心率、血清ANP和血清LDH。此外，它逆转了参与自噬和细胞凋亡的蛋白质的表达，并激活了受 SD 干扰的 PI3K/Akt/mTOR 信号通路。在雷帕霉素诱导的H9c2细胞上，SLSP可以显着恢复异常的自噬和凋亡。总的来说，SLSP 减弱了 SD 诱导的心脏组织中心肌细胞的过度自噬和凋亡，这可能通过激活 PI3K/Akt/mTOR 信号通路起作用。