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已发表论文
人参皂苷 Rg1 通过抑制促炎性巨噬细胞激活减轻肾缺血再灌注损伤和纤维化
Authors Huang Y, Su D, You J, Zhang Y, Li Z, Liu H, Fang Q, Zhi Y , Li W
Received 22 October 2025
Accepted for publication 16 January 2026
Published 4 February 2026 Volume 2026:19 574702
DOI https://doi.org/10.2147/JIR.S574702
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 3
Editor who approved publication: Dr Wenjian Li
Yuandi Huang,1,* Dexi Su,1,* Jinshan You,2 Yu Zhang,1 Zeyu Li,1 Hao Liu,1 Qiang Fang,1 Yi Zhi,1 Weibing Li1
1Department of Urology, The Third Affiliated Hospital of Chongqing Medical University, Chongqing, 401120, People’s Republic of China; 2Department of Hepatobiliary Surgery, The First Affiliated Hospital of Army Medical University, Army Hepatobiliary Surgery Research Institute, Chongqing, 400038, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Yi Zhi, Email urolzhi@hospital.cqmu.edu.cn Weibing Li, Email liweibing63@cqmu.edu.cn
Objective: This study aimed to investigate the protective effects and underlying mechanisms of ginsenoside Rg1 in renal ischemia-reperfusion injury, with a focus on oxidative stress, macrophage polarization, and prevention of early profibrotic responses.
Methods: An in vivo mouse renal IRI model and an in vitro oxygen-glucose deprivation/reperfusion (OGD/R) model using RAW264.7 macrophages were employed to evaluate renal function, oxidative stress, macrophage polarization, pro-inflammatory cytokine expression, and activation of the STING-NF-κB signaling pathway.
Results: Rg1 alleviated renal tubular injury, preserved renal function, and reduced oxidative stress and tubular apoptosis in IRI mice. It also inhibited systemic leukocyte activation and local inflammatory cell infiltration. In vitro, Rg1 suppressed OGD/R-induced M1 polarization, pro-inflammatory cytokine expression, and ROS accumulation, and inhibited activation of the STING-NF-κB signaling pathway. Additionally, Rg1 attenuated early renal fibrosis post-IRI.
Conclusion: Rg1 exerts dual protective effects against renal IRI by reducing oxidative stress and restraining macrophage-mediated inflammation. These findings highlight Rg1 as a promising therapeutic candidate for ischemic kidney injury.
Keywords: Ginsenoside Rg1, renal ischemia-reperfusion injury, acute kidney injury, macrophage polarization, STING-NF-κB pathway, renal fibrosis
1Department of Urology, The Third Affiliated Hospital of Chongqing Medical University, Chongqing, 401120, People’s Republic of China; 2Department of Hepatobiliary Surgery, The First Affiliated Hospital of Army Medical University, Army Hepatobiliary Surgery Research Institute, Chongqing, 400038, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Yi Zhi, Email urolzhi@hospital.cqmu.edu.cn Weibing Li, Email liweibing63@cqmu.edu.cn
Objective: This study aimed to investigate the protective effects and underlying mechanisms of ginsenoside Rg1 in renal ischemia-reperfusion injury, with a focus on oxidative stress, macrophage polarization, and prevention of early profibrotic responses.
Methods: An in vivo mouse renal IRI model and an in vitro oxygen-glucose deprivation/reperfusion (OGD/R) model using RAW264.7 macrophages were employed to evaluate renal function, oxidative stress, macrophage polarization, pro-inflammatory cytokine expression, and activation of the STING-NF-κB signaling pathway.
Results: Rg1 alleviated renal tubular injury, preserved renal function, and reduced oxidative stress and tubular apoptosis in IRI mice. It also inhibited systemic leukocyte activation and local inflammatory cell infiltration. In vitro, Rg1 suppressed OGD/R-induced M1 polarization, pro-inflammatory cytokine expression, and ROS accumulation, and inhibited activation of the STING-NF-κB signaling pathway. Additionally, Rg1 attenuated early renal fibrosis post-IRI.
Conclusion: Rg1 exerts dual protective effects against renal IRI by reducing oxidative stress and restraining macrophage-mediated inflammation. These findings highlight Rg1 as a promising therapeutic candidate for ischemic kidney injury.
Keywords: Ginsenoside Rg1, renal ischemia-reperfusion injury, acute kidney injury, macrophage polarization, STING-NF-κB pathway, renal fibrosis