Objective To investigate the protective effect of metformin on the kidney in type II diabetes mellitus (T2DM) by regulating the activity of poly (ADP-ribose) polymerase 1 (PARP-1) and investigate the mechanism of this effect. Methods Wistar rats were divided into normal group (n = 12), DN group (n = 12), DN + DPQ group (n = 12), DN + metformin group (n = 12) and DN + metformin + DPQ group (n = 12). After model establishment, biochemical parameters such as fasting glucose content, urea nitrogen content, creatinine content, and urine protein concentration were measured in each group of rats. HE staining and TUNEL staining were used to observe the renal pathology, Western blot was applied to detect the protein expression of PARP-1, iNOS, NFκB and caspase-3. The expression of inflammatory factors TNF-α and IL-1β was detected by ELISA, and the expression of 3-nitrotyrosine (3-NT) was determined by immunohistochemistry. Results (1) The biochemical indexes of rats in the three treatment groups decreased compared with those in the DN group, with the most obvious changes in the DN + metformin + DPQ group (P < 0.01); (2) The expression of PARP-1 in rats in the three treatment groups decreased compared to the DN group, with the most significant decrease in the DN + metformin + DPQ group (P < 0.05); (3) The pathological changes of kidney tissue and apoptosis of kidney cells in the three treatment groups were alleviatedcompared with the DN group, with the most significant decrease in the expression of DN + metformin + DPQ group; (4) The expression of inflammatory factors as well as the expression of NF-kB, iNOS and 3-NT decreased in the three treatment groups compared with the DN group, with the most significant decrease in the DN + metformin + DPQ group (P < 0.05). Conclusion Metformin plays a role in protecting the kidney under the high glucose environment caused by diabetes through regulating the expression of PARP-1, downregulating the expression of NF-kB in the DN model, inhibiting NF-kB/iNOS/NO pathway, inhibiting oxidative damage, and reducing inflammation. [ABSTRACT FROM AUTHOR]