Xin Liu, Kanghao Ning, Jiacheng Li, Xiaodong Yan, Juhan Yan, Xinyang Zhao, Xiangdong Li
The First Affiliated Hospital of Hebei North University, Hebei Province, China.
Graduate School of Hebei North University, Hebei Province, China.
Ren Fail. 2025 Dec;47(1):2488140. doi: 10.1080/0886022X.2025.2488140. Epub 2025 Apr 22.
Renal ischemia-reperfusion injury (RIRI) is a common cause of acute renal injury. Studies have shown that sodium aescinate (SA) may serve as a potential therapeutic agent, although its exact mechanism remains unclear. This study first evaluated the efficacy of SA using a mouse renal ischemia-reperfusion model. Subsequently, its mechanism was elucidated through systematic bioinformatics, and finally validated through and experiments. The results demonstrated that SA has a protective effect on renal function in mice with RIRI. Bioinformatic analysis indicated that the pyroptosis pathway is significantly activated during renal ischemia-reperfusion injury, and immunohistochemistry showed that the level of renal pyroptosis is upregulated during ischemia-reperfusion injury. Administration of SA was able to reduce the expression of pyroptosis-related proteins (GSDMD, NLRP3, IL-1β) in RIRI. and experiments further confirmed that SA exerts an anti-pyroptotic effect by inhibiting the AKT/NLRP3 signaling pathway. Ultimately, SA mitigates kidney injury in IRI mice by suppressing renal failure through inhibition of the AKT/NLRP3 signaling pathway.
肾缺血再灌注损伤（RIRI）是急性肾损伤的常见原因。研究表明，七叶皂苷钠（SA）可能是一种潜在的治疗药物，但其确切机制尚不清楚。本研究首先使用小鼠肾缺血再灌注模型评估了SA的疗效。随后，通过系统的生物信息学阐明其机制，最后通过[具体实验1]和[具体实验2]实验进行验证。结果表明，SA对RIRI小鼠的肾功能具有保护作用。生物信息学分析表明，在肾缺血再灌注损伤期间，焦亡途径被显著激活，免疫组织化学显示，在缺血再灌注损伤期间，肾焦亡水平上调。给予SA能够降低RIRI中焦亡相关蛋白（GSDMD、NLRP3、IL-1β）的表达。[具体实验1]和[具体实验2]实验进一步证实，SA通过抑制AKT/NLRP3信号通路发挥抗焦亡作用。最终，SA通过抑制AKT/NLRP3信号通路抑制肾衰竭，从而减轻IRI小鼠的肾损伤。
