The key regulators of diabetic nephropathy (DN) are oxidative tissue damage and inflammatory response. We used a rat model of hyperglycemia-induced kidney injury to investigate the potential protective effect of bisacurone. A diabetic rat model was established by injecting 50 mg kg-1 of streptozotocin (STZ) intraperitoneally. Bisacurone oral dosages of 50 and 100 mg/kg were administered to rats for eight weeks. In-creases in blood creatinine, blood urea nitrogen (BUN), and urine albumin were seen in diabetic rats, as were elevations in glucose and glycosylated haemoglobin levels in these animals. Malondialdehyde and protein carbonyl levels rose in the kidneys of rats with DN, but superoxide dismutase, catalase, and reduced glutathione levels fell. The protein expression and mRNA levels of pro-inflammatory cytokines (such as tumour necrosis factor-a, interleukin-1 beta, and interleukin-6) were also increased in DN rats. Treatment with bisacurone effectively decreased hyperglycemia, improved renal function, decreased oxidative stress and inflammation, and increased antioxidants in the kidneys. Our result demonstrated that bisacurone had nephroprotective activity in STZ-induced diabetic rats. The potential therapeutic benefits of bisacurone in the treatment of DN need further study in controlled clinical studies.