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<p>Septic cardiomyopathy (SCM) is a severe complication of sepsis. The therapeutic potential of Ginsenoside Rh4 (Rh4) in SCM remains unclear. This study aimed to investigate the effects and mechanisms of Rh4 on SCM using both in vivo and in vitro approaches. In the in vivo experiments, Rh4 significantly reduced the mortality rate in SCM mice, improved ejection fraction and diastolic function, and protected myocardial cell mitochondria, thereby alleviating myocardial cell injury. Transcriptomic sequencing, ELISA, and PCR results suggested that Rh4 reduced inflammatory cytokines in myocardial tissues, likely through the inhibition of the NF-κB signaling pathway. This effect was associated with a reduction in pro-inflammatory M1 macrophages and an increase in the proportion of reparative M2 macrophages. Additionally, Rh4 alleviated myocardial cell apoptosis and attenuated myocardial fibrosis at later stages. In vitro, we found that Rh4 reduced LPS-induced macrophage polarization and promoted the polarization of macrophages into anti-inflammatory M2 macrophages. Moreover, flow cytometry analysis revealed that Rh4 decreased reactive oxygen species (ROS) production in HL-1 cardiomyocytes, with the mechanism linked to the activation of the Keap1/Nrf2/HO-1 signaling pathway. Finally, Rh4 treatment significantly inhibited the pro-apoptotic effects of LPS on HL-1 cells. In conclusion, Rh4 improves heart function by reducing macrophage polarization and ROS generation, protecting myocardial cell mitochondria, and reducing myocardial cell apoptosis.</p>

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Ginsenoside Rh4-regulated macrophage polarization and oxidative stress in septic myocardial injury

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月18日

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  • Bingxin Huang,
  • Yue Tang,
  • Xinpeng Jiang,
  • Hongtao Shen,
  • Yidi Yang,
  • Ling Jing,
  • Hang Yang,
  • Yunpeng Ling,
  • Mowei Song

摘要

Septic cardiomyopathy (SCM) is a severe complication of sepsis. The therapeutic potential of Ginsenoside Rh4 (Rh4) in SCM remains unclear. This study aimed to investigate the effects and mechanisms of Rh4 on SCM using both in vivo and in vitro approaches. In the in vivo experiments, Rh4 significantly reduced the mortality rate in SCM mice, improved ejection fraction and diastolic function, and protected myocardial cell mitochondria, thereby alleviating myocardial cell injury. Transcriptomic sequencing, ELISA, and PCR results suggested that Rh4 reduced inflammatory cytokines in myocardial tissues, likely through the inhibition of the NF-κB signaling pathway. This effect was associated with a reduction in pro-inflammatory M1 macrophages and an increase in the proportion of reparative M2 macrophages. Additionally, Rh4 alleviated myocardial cell apoptosis and attenuated myocardial fibrosis at later stages. In vitro, we found that Rh4 reduced LPS-induced macrophage polarization and promoted the polarization of macrophages into anti-inflammatory M2 macrophages. Moreover, flow cytometry analysis revealed that Rh4 decreased reactive oxygen species (ROS) production in HL-1 cardiomyocytes, with the mechanism linked to the activation of the Keap1/Nrf2/HO-1 signaling pathway. Finally, Rh4 treatment significantly inhibited the pro-apoptotic effects of LPS on HL-1 cells. In conclusion, Rh4 improves heart function by reducing macrophage polarization and ROS generation, protecting myocardial cell mitochondria, and reducing myocardial cell apoptosis.