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Acute kidney injury (AKI) is a critical care syndrome, which is usually associated with sepsis-related endotoxemia. Evodiamine (EVO) is an active ingredient of many traditional medicinal formulations that possess a battery of biological activities. In the study, we aimed to evaluate the potential protective effect of EVO against lipopolysaccharide- (LPS-) induced AKI and cytotoxicity. LPS-resulted pathological injuries were significantly ameliorated by the administration of EVO. EVO reduced the levels of blood urea nitrogen (BUN) and creatinine in LPS-treated rats. EVO also inhibited LPS-induced reduction of cell viability in NRK-52E cells. LPS-resulting increase of TNF α  and IL-1 β  in both serum and kidney of rats and NRK-52E cells was inhibited by EVO. LPS-induced increase of P65 NF- κ B expression was markedly inhibited by EVO. EVO-induced reduction of TNF α  and IL-1 β  expression in LPS-treated cells was blocked by overexpression of P65 NF- κ B. Moreover, the increase of cell viability in LPS-treated cells induced by EVO was remarkably suppressed by overexpression of P65 NF- κ B. LPS-resulting increase of reactive oxygen species (ROS) production was suppressed by EVO. H 2 O 2  suppressed EVO-induced decrease of P65 NF- κ B expression and increase of cell viability in LPS-treated NRK-52E cells. Moreover, the antioxidant NAC significantly promoted EVO-induced decrease of P65 NF- κ B expression and increase of cell viability in LPS-treated NRK-52E cells. In conclusion, EVO had crucial protective effects against LPS-induced AKI and cytotoxicity through the antioxidant activities and thus the inhibition of inflammation. Our data highlight EVO as a potential candidate for the development of new strategies for the treatment of AKI.

Protective Effects of Evodiamine against LPS-Induced Acute Kidney Injury through Regulation of ROS-NF-κB-Mediated Inflammation