急性肾损伤（AKI）是一种可以由不同因素引起的并发症。大蒜素是一类具有抗癌和抗菌效果的有机硫化合物，在脓毒症诱发的S-AKI（脓毒症相关急性肾损伤）中尚未报道。通过盲肠结扎穿孔法在c57BL/6小鼠中诱发了S-AKI。在大蒜素治疗的作用下，S-AKI小鼠的存活率提高。降低的血清肌酐、血尿素氮、尿白蛋白、KIM-1和NGAL水平表明S-AKI小鼠肾功能改善。大蒜素抑制了炎症和细胞凋亡，通过降低炎症因子和相关蛋白的水平来证明。通过氧化应激生物标志物的水平来评估氧化应激，并被大蒜素抑制。此外，通过减少JC-1绿色单体来表征大蒜素减轻的线粒体功能障碍。这些大蒜素的效应也在用脂多糖（LPS）处理的HK2细胞中得到证实。在体内和体外实验中，显示出大蒜素治疗后Nrf2核转位以及HO-1表达增加，这通过ML385和CDDO-Me得到了证实。综上所述，本研究揭示了大蒜素对S-AKI的缓解作用，并首次证明了大蒜素对Nrf2核转位的促进作用。研究推断大蒜素通过Nrf2/HO-1信号通路抑制了S-AKI的进展。本研究对于理解大蒜素在S-AKI中的作用具有重要意义。 © 2023. 作者。

Acute kidney injury (AKI) is a complication that can be induced by different factors. Allicin is a class of organic sulfur compounds with anticancer and antibacterial effects, and has not been reported in sepsis-induced AKI (S-AKI). S-AKI was induced in c57BL/6 mice by cecal ligation puncture. In response to the treatment of allicin, the survival rate of mice with S-AKI was increased. Reduced levels of serum creatinine, blood urea nitrogen, UALB, KIM-1 and NGAL indicated an improvement in renal function of S-AKI mice. Allicin inhibited the inflammation and cell apoptosis, which evidenced by decreased levels of inflammatory cytokines and apoptosis-related proteins. Oxidative stress was evaluated by the levels of oxidative stress biomarkers, and suppressed by allicin. In addition, allicin-alleviated mitochondrial dysfunction was characterized by decreased JC-1 green monomer. These effects of allicin were also evidenced in HK2 cells primed with lipopolysaccharide (LPS). Both in vivo and in vitro experiments showed that the nuclear translocation of Nrf2 and the expression of HO-1 increased after allicin treatment, which was confirmed by ML385 and CDDO-Me. In summary, this study revealed the alleviating effect of allicin on S-AKI and demonstrated the promotive effect of allicin on nuclear translocation of Nrf2 for the first time. It was inferred that allicin inhibited the progression of S-AKI through Nrf2/HO-1 signaling pathway. This study makes contributions to the understanding of the roles of allicin in S-AKI.© 2023. The Author(s).