Septic acute kidney injury (AKI) characterized as acute infection and renal inflammation, still lacks of effective therapies. Isoliquiritigenin (ISL) as a small molecular from licorice, is able to inhibit the expression of HMGB1. However, the role and mechanism of ISL in septic AKI has not been investigated. In this study, we used LPS injection to induce murine septic AKI. One hour before LPS injection, 50 mg/kg ISL was once orally given to the mice. For the in vitro study, HK2 human tubular cells were respectively treated with 50 μM and 100 μM ISL 5 hrs before 2 μg/ml LPS stimulation. Then we observed that ISL ameliorated renal dysfunction and attenuated renal tubular injury. ISL inhibited the phosphorylation of IκB-α and NF-κB p65 after LPS induction both in vivo and in vitro. ISL also inhibited NF-κB p65 translocation from cytoplasm to the nucleus upon LPS stimulation. Further, NF-κB p65 translocation could trigger macrophage polarization, neutrophil activation and pro-inflammatory cytokines secretion in LPS-induced inflammation. These results showed that ISL could alleviate LPS-induced AKI by suppressing NF-κB p65 translocation and inhibiting inflammatory responses, indicating protective effects of ISL in LPS-induced acute renal inflammation. This study might be useful for designing potential clinical trials to prevent and treat sepsis induced AKI in patients with serious illness.
Keywords: NF-κB p65; Septic acute kidney injury; inflammation response; isoliquiritigenin.