Jinzhong Wang M S, Jian Fu M S
Department of Critical Care Medicine, The Second Affiliated Hospital of Hainan Medical University, No. 48. Baishuitang Road, Haikou City, Hainan province, 570311, China.
Department of Infectious Disease, Hainan General Hospital, Hainan Medical University, Haikou, Hainan, 570311, China.
J Mol Histol. 2025 Apr 28;56(3):148. doi: 10.1007/s10735-025-10417-3.
This study explored the role and mechanism of action of ginsenoside Rc in treating septic cardiomyopathy. Ginsenoside Rc mitigated LPS-induced oxidative stress, inflammation, apoptosis, and mitochondrial dysfunction in cardiomyocytes and inhibited M1 polarization in macrophages. Ginsenoside Rc reduced the stimulating effect of M1-polarized macrophages on LPS-induced cardiomyocyte injury. Network pharmacological analysis suggested that ginsenoside Rc may play a role in septic cardiomyopathy through modulation of the STAT3/FoxO3a/Sirt1 pathway, which was validated in in vitro experiments. Ginsenoside Rc suppressed the expression of STAT3/FoxO3a pathway proteins and upregulated Sirt1. Moreover, influences of ginsenoside Rc on LPS-induced cardiomyocyte injury and macrophage polarization were abolished by ML115, a STAT3 agonist. In vivo, ginsenoside Rc notably improved myocardial injury and attenuated macrophage activation and inflammation in septic mice. Collectively, Ginsenoside Rc can ameliorate septic cardiomyopathy by modulating the STAT3/FoxO3a/Sirt1 pathway and altering macrophage polarization.
本研究探讨了人参皂苷Rc在治疗脓毒症性心肌病中的作用及作用机制。人参皂苷Rc减轻了脂多糖（LPS）诱导的心肌细胞氧化应激、炎症、凋亡和线粒体功能障碍，并抑制了巨噬细胞的M1极化。人参皂苷Rc降低了M1极化巨噬细胞对LPS诱导的心肌细胞损伤的刺激作用。网络药理学分析表明，人参皂苷Rc可能通过调节STAT3/FoxO3a/Sirt1通路在脓毒症性心肌病中发挥作用，这在体外实验中得到了验证。人参皂苷Rc抑制了STAT3/FoxO3a通路蛋白的表达并上调了Sirt1。此外，STAT3激动剂ML115消除了人参皂苷Rc对LPS诱导的心肌细胞损伤和巨噬细胞极化的影响。在体内，人参皂苷Rc显著改善了脓毒症小鼠的心肌损伤，减轻了巨噬细胞活化和炎症。总的来说，人参皂苷Rc可通过调节STAT3/FoxO3a/Sirt1通路和改变巨噬细胞极化来改善脓毒症性心肌病。
