Isovitexin protects against cisplatin-induced kidney injury in mice through inhibiting inflammatory and oxidative responses

•Isovitexin significantly reduced the increase in serum BUN and creatinine induced by CP.•CP-induced TNF-α, IL-1ß and IL-6 in kidney tissues were also inhibited by isovitexin.•Isovitexin inhibited CP-induced oxidative stress by inhibiting MDA and ROS production.•Isovitexin was found to inhibit CP-induced NF-κB activation and increase Nrf2 and HO-1 expression. In this study, we investigated the renoprotective effects and mechanism of isovitexin, a glycosylflavonoid isolated from rice hulls of Oryza sativa, against cisplatin-induced kidney injury in mice. The mice were treated with cisplatin for four consecutive days and at the second day, the mice were received with isovitexin for three consecutive days. The levels of blood urea nitrogen (BUN) and creatinine in serum and the levels of MDA, ROS, TNF-α, IL-1ß and IL-6 in kidney tissues were measured. The proteins of Nrf2 and NF-κB signaling pathways were measured by western blot analysis. Our results demonstrated that isovitexin inhibited CP-induced increases in serum BUN and creatinine. Isovitexin inhibited CP-induced inflammation by inhibiting TNF-α, IL-1ß and IL-6 production in kidney tissues. Also, isovitexin inhibited CP-induced oxidative stress by inhibiting MDA and ROS production. Furthermore, isovitexin was found to inhibit CP-induced NF-κB activation and increase Nrf2 and HO-1 expression. In conclusion, our results indicated that isovitexin protected against CP-induced kidney injury by suppressing inflammatory and oxidative responses.