〔Abstract〕 Objective To investigate the effects of carnosine(CAR) on streptozotocin(STZ) induced renal ferroptosis and inflammation in diabetic mice. Methods Type 1 diabetes mice model were induced by STZ, and normal C57 mice were used as normal control group. The C57 mice were divided into 5 groups(6-8 mice in each group): normal control group(NC), normal control + carnosine group(NC+CAR), STZ model group(STZ), STZ model + carnosine group(STZ+CAR), STZ model + ferroptosis inhibitor group(STZ+Fer-1). After feeding the mice for 16 weeks, serum samples were collected to detect blood creatinine(CRE) and urea nitrogen(BUN) levels. The urine of mice was collected to detect the 24-hour urinary albumin level. HE staining and PAS staining were performed to observe the degree of renal pathological injury. Real-time PCR was used to detect the expression of interleukin(IL)-1β, IL-6,monocyte chemotactic protein 1(MCP-1) and tumor necrosis factor-α(TNF-α) in mouse kidney tissue. The expression of reactive oxygen species(ROS) in mouse kidney was detected by immunofluorescence.Morphology of renal mitochondria was observed by transmission electron microscopy. The protein expression levels of glutathione peroxidase 4(GPX 4) and long-chain lipoacyl-CoA synthetase 4(ACSL4), which are ferroptosis indexes, were detected by Western blot. The contents of malondialdehyde(MDA), glutathione(GSH) and Fe2+in mouse kidney tissue were determined. Results Compared with NC group, CRE and BUN levels in STZ group increased(P<0.001); and ompared with STZ group, these indexes decreased in STZ+CAR group(P<0.001,P<0.01). Renal histopathological examination showed that compared with NC group, renal tubule dilatation, inflammatory cell infiltration and glycogen deposition significantly increased in STZ group; and compared with STZ group, tubule dilatation, inflammatory cell infiltration and glycogen deposition decreased in STZ+CAR group. Electron microscope results showed that the renal mitochondria in STZ group were swollen, membrane density increased, mitochondrial ridges decreased or absent, renal tubule dilation was improved significantly in the STZ+CAR group and STZ+Fer-1 group, and inflammatory cell infiltration was reduced. Real-time PCR test results showed that compared with NC group, mRNA expression levels of inflammatory factor(IL-1β, IL-6, MCP-1 and TNF-α) increased in STZ group(P<0.001 orP<0.01); and mRNA expressions of IL-1β, IL-6, MCP-1 and TNF-α were decreased in STZ+CAR group compared with STZ group(P<0.01 orP<0.05). Immunofluorescence results showed that compared with NC group, ROS level in kidney tissue of mice in STZ group increased(P<0.001); and compared with STZ group, the expression of ROS in kidney tissue of STZ+CAR group decreased while ROS expression in STZ+CAR group decreased(P<0.01). Compared with NC group, GPX4 expression and GSH content in kidney of STZ group decreased(P<0.001), and ACSL4 protein expression and MDA and Fe2+contents increased(P<0.01 orP<0.001), GPX4 expression and GSH content increased(P<0.01), ACSL4 protein expression and MDA and Fe2+content decreased in STZ+CAR group(P<0.01 orP<0.001). Conclusion CAR inhibits ferroptosis and inflammation in the kidney in diabetic mice induced by STZ, and improved renal pathological injury in diabetic mice.