Eleutherococcus senticosus (ES) exerts various pharmacological effects, including renoprotection in a rat model of renal ischemia-reperfusion injury. However, the mechanisms of these effects remain unclear. Therefore, we investigated the effects and mechanisms of ES on aristolochic acid (AA)-induced acute kidney injury in mice. The experimental mice were divided into the control group, the model group (AA-induced acute kidney injury model), the model + ES group (Eleutherococcus senticosus boiled-free granules treated by gavage for two weeks), the model + fasudil group (fasudil administered intraperitoneally for three days), and the model + ES + fasudil group. After AA intervention in normal mice, the expression of ASC and NLRP3 and the levels of IL-1β, IL-18, and TNF-α were significantly elevated in mouse renal tissues (P < 0.05). However, AA-induced renal dysfunction was ameliorated by both ES and fasudil, which was confirmed by the decrease in serum creatinine and blood urea nitrogen levels, as well as by renal histopathological abnormalities such as renal tubule dilation and tubular formation. In addition, the inflammatory response of AA-induced renal inflammation was inhibited by both ES and fasudil, and the expression of ASC and NLRP3 and the levels of IL-1β, IL-18, and TNF-α were significantly higher in mouse renal tissues after the treatment of either ES or fasudil (P < 0.05). ES may be a potential treatment agent for aristolochic-acid-triggered nephropathy, with inhibition of the NLRP3/IL-1β as one plausible underlying mechanism.

中文翻译：

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Eleutherococcus senticosus 通过抑制小鼠 NLRP3/IL-1β 信号通路减轻马兜铃酸诱导的急性肾损伤

Eleutherococcus senticosus （ES） 在肾缺血再灌注损伤大鼠模型中发挥多种药理作用，包括肾脏保护。然而，这些影响的机制仍不清楚。因此，我们研究了 ES 对马兜铃酸 （AA） 诱导的小鼠急性肾损伤的影响和机制。将实验小鼠分为对照组、模型组（AA 诱导的急性肾损伤模型）、模型+ES 组（刺五叶球菌无煮颗粒灌胃处理 2 周）、模型+法舒地尔组（法舒地尔腹膜内给药 3 d）和模型+ES+法舒地尔组。正常小鼠 AA 干预后，小鼠肾组织中 ASC 和 NLRP3 表达以及 IL-1β 、 IL-18 和 TNF-α 水平显著升高 （P < 0.05）。然而，ES 和法舒地尔均改善了 AA 诱导的肾功能不全，这可以通过血清肌酐和血尿素氮水平的降低以及肾组织病理学异常（如肾小管扩张和肾小管形成）来证实。此外，ES 和法舒地尔均抑制了 AA 诱导的肾脏炎症的炎症反应，ES或法舒地尔治疗后小鼠肾组织中ASC和NLRP3的表达以及IL-1β、IL-18和TNF-α水平显著升高（P < 0.05）。ES 可能是马兜铃酸触发的肾病的潜在治疗剂，抑制 NLRP3/IL-1β 是一种可能的潜在机制。