Backgrounds

Contrast-induced acute kidney injury (CIAKI) is the third most common cause of hospital-acquired AKI. It has been demonstrated that microRNA-30c (miR-30c) was upregulated in the CIAKI. However, the underlying mechanism remain unclear.

Methods

The CIAKI was induced in miniature pig. The expression profile of miR-30c in the kidney was evaluated by qPCR. The pathways regulated by miR-30c was identified by qPCR and western blot on renal tubular epithelial cells isolated from miniature pig. Finally, the potential therapeutic application of targeting miR-30c was assessed in the pig model of CIAKI.

Results

The miR-30c was up-regulated in miniature pig with CIAKI. The miR-30c suppressed cell apoptosis, expression of NLRP3, the secretion of IL-1β and caspase-1 p10 on renal cells stimulated by iohexol in vitro. In the pig model, miR-30c inhibited the CIAKI development.

Conclusion

Our data demonstrated that the miR-30c induced by CIAKI could suppress cell apoptosis and kidney injury via targeting NLRP3. Therefore, targeting miR-30c might be a novel therapeutic candidate for CIAKI treatment and prevention.

中文翻译：

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MicroRNA-30c通过抑制NLRP3炎症小体来减轻造影剂引起的急性肾脏损伤。

背景资料

造影剂引起的急性肾损伤（CIAKI）是医院获得性AKI的第三大最常见原因。已经证明在CIAKI中microRNA-30c（miR-30c）被上调。但是，其潜在机制仍不清楚。

方法

CIAKI是在小型猪中诱导的。通过qPCR评估miR-30c在肾脏中的表达谱。在分离自小型猪的肾小管上皮细胞上，通过qPCR和Western blot鉴定了miR-30c调控的途径。最后，在CIAKI的猪模型中评估了靶向miR-30c的潜在治疗应用。

结果

CIAKI在微型猪中上调了​​miR-30c。miR-30c抑制了碘海醇在体外刺激肾细胞的细胞凋亡，NLRP3表达，IL-1β和caspase-1 p10的分泌。在猪模型中，miR-30c抑制了CIAKI的发育。

结论

我们的数据表明，CIAKI诱导的miR-30c可通过靶向NLRP3抑制细胞凋亡和肾脏损伤。因此，靶向miR-30c可能是CIAKI治疗和预防的新型治疗候选药物。