Isoliquiritigenin attenuates LPS-induced AKI by suppression of inflammation involving NF-κB pathway.
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ABSTRACT: 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
SUBMITTER: Tang Y
PROVIDER: S-EPMC6325500 | biostudies-literature | 2018
REPOSITORIES: biostudies-literature
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