OBJECTIVE： To study the protective effect of tanshinone ⅡA（TSⅡA） sulfonate injection against vancomycin （VAN）- induced renal injury model rats and its mechanism. METHODS： 72 rats were randomly divided into blank group， model group， positive control group （amifostine， 1 mg/kg） and TSⅡA sulfonate injection low-dose， medium-dose and high-dose groups （15， 30， 60 μg/kg）， with 12 rats in each group. Except for blank group， those groups were given VAN （200 mg/kg） intravenously via tail vein to induce renal injury rat model； after modeling， each drug group was given relevant medicine intraperitoneally once a day， and blank group and model group were given normal saline intragastrically for consecutive 10 days. The levels of 24 h protein， NAG and KIM-1 in urine were determined， and those of Cys C， Scr and BUN in serum and those of SOD， MDA， GSH-Px and NO in renal homogenate were also determined； the pathological change of renal tissue was observed. RESULTS： Compared with blank group， the levels of Cys C， Scr and BUN in serum， those of 24 h protein， NAG and KIM-1 in urine and those of MDA and NO in renal tissue increased significantly in model group， while the levels of SOD and GSH-Px decreased significantly （P＜0.01）； the pathological slice indicated that model group suffered from renal injury such as kidney tubules albuminoid degeneration， brush border abscission， renal tubular epithelial cell disintegration and abscission. Compared with model group， the levels of Cys C， Scr and BUN in serum， those of 24 h protein， NAG and KIM-1 in urine and those of MDA and NO in renal tissue decreased significantly in treatment groups， while the levels of SOD and GSH-Px in renal tissue increased significantly （P＜0.05 or P＜0.01）； pathological changes of renal tissue were relieved significantly. CONCLUSIONS： TSⅡA sulfonate injection can effectively relieve VAN-induced renal injury in rats， and its mechanism may be associated with inhibiting the oxidative reaction of rats in vivo.