Sepsis-induced acute kidney injury (SAKI) is a common complication of hospitalized patients, often leading to unacceptable mortality. Limited effective treatment or diagnosis biomarkers are available and the underlying mechanism remains unclear. The miR-30c-5p is considered as a critical mediator of kidney diseases and aberrantly decreased in patients with SAKI, while the mechanism is still unclear. For this purpose, the role of miR-30c-5p in SAKI has been investigated in this study. Here, we first confirmed that miR-30c-5p expression decreased in our septic models and was associated with the activation of NLRP3/caspase-1-mediated pyroptosis. Overexpression of miR-30c-5p alleviated the kidney injury via suppressing HK-2 cell pyroptosis. Furthermore, we identified that TXNIP was a direct target of miR-30c-5p. Upregulation of miR-30c-5p repressed the expression of TXNIP, which inhibited NLRP3, ASC, and caspase-1 expression, as well as secretion of inflammatory cytokines. In conclusion, our data suggested that miR-30c-5p negatively controlled the NLRP3 signal pathway-related pyroptosis and sepsis-induced injury via TXNIP, indicating that this axis might be a positive therapeutic target for the patient with SAKI.

脓毒症引起的急性肾损伤 (SAKI) 是住院患者的常见并发症，通常会导致不可接受的死亡率。可用的有效治疗或诊断生物标志物有限，潜在机制仍不清楚。miR-30c-5p 被认为是肾脏疾病的关键介质，在 SAKI 患者中异常降低，但其机制尚不清楚。为此，本研究调查了 miR-30c-5p 在 SAKI 中的作用。在这里，我们首先证实 miR-30c-5p 表达在我们的脓毒症模型中降低，并且与 NLRP3/caspase-1 介导的细胞焦亡的激活有关。miR-30c-5p的过表达通过以下方式减轻肾损伤抑制 HK-2 细胞焦亡。此外，我们确定 TXNIP 是 miR-30c-5p 的直接靶标。miR-30c-5p 的上调抑制了 TXNIP 的表达，从而抑制了 NLRP3、ASC 和 caspase-1 的表达，以及炎性细胞因子的分泌。总之，我们的数据表明 miR-30c-5p 通过 TXNIP 对 NLRP3 信号通路相关的细胞焦亡和败血症诱导的损伤进行负控制，表明该轴可能是 SAKI 患者的阳性治疗靶点。