It is well known that the local renin-angiotensin system (RAS) is activated in the diabetic state, which results in an increase in the level of oxidative stress injury to pancreatic β cells. The angiotensin‑converting enzyme 2 (ACE2)/angiotensin (1‑7) [Ang (1‑7)]/Mas axis is a negative regulator of the classical renin‑angiotensin system. In order to investigate the antioxidant effect of Ang (1‑7) on pancreatic β cells, INS‑1 cells were cultured and oxidative stress was induced by treatment with H2O2. Glucose‑stimulated insulin secretion (GSIS), the generation of reactive oxygen species (ROS), mitochondrial membrane potential (MMP) and glucose-stimulated calcium (GSCa) responses in β cells were determined following treatment with Ang (1-7). It was observed that H2O2 significantly impaired the insulin secreting function, increased the production of ROS, and also decreased the levels of GSCa and MMP. Pre‑treatment with Ang (1‑7) alleviated these effects and treatment with A779 [antagonist of Ang (1‑7)] prevented the effects of Ang (1-7). Based on these findings, it was concluded that Ang (1‑7) can protect pancreatic β cells from oxidative injury and such protection can be blocked by its antagonist A779.