Objective: To investigate the role of relaxin in acute kidney injury and fibrosis induced by ischemia-reperfusion in mice. Methods: Mice were divided into four experimental groups: sham-operated animal group (sham), sham-operated animals receiving relaxin-treated group (sham + relaxin), ischemia-reperfusion mice group (IRI), and ischemia-reperfusion mice receiving relaxin treatment group (IRI + relaxin). After establishing the model of ischemia-reperfusion injury in mice, the level of creatinine was detected by ELISA assay. HE staining was used to observe the degree of renal tissue damage. The expression levels of α-SMA and Desmin in renal fibrosis were detected by immunohistochemistry method. Collagen deposition was detected by day-stained red staining. The expression levels of representative antigen F4/80 and ly6g which are represent of neutrophils and macrophages infiltrated were detected by immunohistochemistry. Results: Creatinine was significantly elevated in the IRI group (P<0.001), but decreased in the IRI + relaxin group (P<0.01). The results of HE staining showed an increased renal injury in the IRI group (P<0.001) and a decrease in the IRI + relaxin group (P<0.01). The same results of immunohistochemistry showed that the fibrosis index was significantly increased in the IRI group (P<0.001), and decreased in the IRI + relaxin group (P<0.01). Inflammatory infiltration of neutrophils and macrophages showed the same results. Conclusion: Relaxin can attenuate acute kidney injury and fibrosis in mice induced by ischemia-reperfusion.