Objective To investigate and explore the potential mechanism of the protective effects of artesunate on adriamycin-induced kidney injury in rats. Methods Thirty-two male Wistar rats were randomly divided into four groups of 8 rats each: negative control ( NC), kidney injury model ( ADR), low-dose artesunate ( ART-L), and high-dose artesunate (ART-H). The model group, ART-L and ART-H treatment groups received a single tail vein injection of adriamycin (7. 5 mg / kg body weight).After modeling, the rats in the treatment groups were given 25 mg / kg (ART-L) and 50 mg / kg (ART-H) artesunate, intragastrically for 3 consecutive weeks. The NC and ADR groups were injected with isotonic saline. Blood urea nitrogen ( BUN) and serum creatinine ( Scr) were measured by an automatic biochemical analyzer. Hematoxylin and eosin ( HE) staining was used to observed renal morphological changes. Kits were used to measure the levels of superoxide dismutase ( SOD), malondialdehyde (MDA) and glutathione peroxidase (GSH-Px) in renal tissues of rats in each group. Results Serum levels of BUN and Scr, and the content of MDA in renal tissues were significantly higher in the ADR group than the NC group (P< 0. 01), while the serum levels of ALB and the activities of SOD and GSH-Px in renal tissues were significantly lower (P< 0. 01). Compared with the ADR group, serum levels of BUN and Scr, and the content of MDA in renal tissues were significantly lower in the ART-L and ART-H groups, while the serum levels of ALB and the activities of SOD and GSH-Px in renal tissues were significantly higher ( P< 0. 01). HE staining revealed that artesunate reduced renal injury induced by adriamycin. Conclusions Artesunate reduced urine protein in rats with adriamycin-induced kidney injury, improving renal function and pathological tissue damage. The underlying mechanism may be related to the inhibition of oxidative stress induced by adriamycin in renal tissue.