Curcumin alleviates septic acute kidney injury (SAKI); however, the underlying mechanism remained unclear. To explore this, SAKI cell model and mice model were conducted by using LPS and cecal ligation and puncture (CLP), respectively. Cell counting kit-8 (CCK-8) and enzyme-linked immunosorbent assay (ELISA) assays indicated that LPS reduced the viability, but upregulated the levels of tumor necrosis factor (TNF)-α and interleukin (IL)-6, whereas Curcumin pretreatment had no effect on viability, but reduced the levels of TNF-α and IL-6. Further assays showed that Curcumin partly attenuated the LPS-induced injury as the viability was enhanced, TNF-α and IL-6 expressions and cell apoptosis rates were reduced. Western blot analysis indicated that Janus kinase (JAK) 2/signal transducer and activator of transcription (STAT) 3, p-65-NF-κB and cell apoptosis pathways were activated by LPS but suppressed by Curcumin. Mice SAKI model further indicated that the serum Cystatin C (Cys-C), creatinine (Cr) and blood urea nitrogen (BUN) were increased within 24 h of model construction while those indicators were decreased at 48 h. Pretreated with Curcumin, NF-κB inhibitor (PDTC) or JAK2 inhibitor (AG-490) could weaken the renal histological injury and the increased serum Cys-C, Cr and BUN, IL-6 and TNF-α induced by CLP. Moreover, PDTC, AG-490 and Curcumin all significantly reversed the previously increased expressions of p-JAK2/STAT3, p-p65 and proapoptotic proteins in the mice with AKI. The present study revealed that Curcumin attenuated SAKI through inhibiting NF-κB and JAK2/STAT3 signaling pathways, and proposed that Curcumin could be a potential therapeutic agent for treating SAKI.

姜黄素减轻脓毒性急性肾损伤 (SAKI)；然而，潜在的机制仍不清楚。为了探索这一点，分别使用 LPS 和盲肠结扎穿孔 (CLP) 进行了 SAKI 细胞模型和小鼠模型。细胞计数试剂盒-8 (CCK-8) 和酶联免疫吸附测定 (ELISA) 测定表明 LPS 降低了生存能力，但上调了肿瘤坏死因子 (TNF)-α 和白细胞介素 (IL)-6 的水平，而姜黄素预处理对生存力没有影响，但降低了 TNF-α 和 IL-6 的水平。进一步的分析表明，姜黄素部分减轻了 LPS 诱导的损伤，因为活力增强，TNF-α 和 IL-6 表达和细胞凋亡率降低。蛋白质印迹分析表明，Janus 激酶 (JAK) 2/信号转导和转录激活因子 (STAT) 3，p-65-NF-κB 和细胞凋亡通路被 LPS 激活但被姜黄素抑制。小鼠SAKI模型进一步表明，模型构建24 h内血清胱抑素C（Cys-C）、肌酐（Cr）和血尿素氮（BUN）升高，而这些指标在48 h下降。姜黄素、NF-κB抑制剂（PDTC）或JAK2抑制剂（AG-490）预处理可减弱CLP诱导的肾组织损伤和血清Cys-C、Cr和BUN、IL-6和TNF-α的升高。此外，PDTC、AG-490 和姜黄素都显着逆转了 AKI 小鼠先前增加的 p-JAK2/STAT3、p-p65 和促凋亡蛋白的表达。本研究表明姜黄素通过抑制 NF-κB 和 JAK2/STAT3 信号通路减弱 SAKI，