The impaired proliferative capacity of alveolar epithelial cells after injury is often an important factor causing epithelial repair dysfunction, leading to the occurrence of lung diseases such as idiopathic pulmonary fibrosis (IPF). Lipocalin-2 (LCN2) participates in multiple processes regulating the pathological process of alveolar epithelial cells, but the mechanisms involved are still unclear. We used bleomycin (BLM)-treated mouse model to characterize the expression of LCN2 in the lung fibrosis regions and analyzed the location of LCN2 in alveolar epithelial cells. LCN2 was increased in the alveolar epithelium post-BLM injury, and highly expressed LCN2 was mainly concentrated on alveolar type 2 (AT2) cells in BLM-injured lungs. Moreover, human pulmonary alveolar epithelial cells (HPAEpiCs) were transfected with the LCN2 overexpression plasmid vector in vitro, LCN2-overexpressing HPAEpiCs showed impaired cell viability and cell growth. Recombinant human interleukin 17 (IL-17) protein (rhIL-17) at different concentrations was administered to intervene HPAEpiCs and observe cell viability and cell growth state and to analyze the concentration-dependent effect of IL-17. HPAEpiC intervention with rhIL-17 mildly rescued the impaired cell proliferation induced by LCN2 overexpression, and the effect of IL-17 intervention was partially concentration dependent. The target cells regulated by this process were Pro-surfactant protein C (Prospc) positive alveolar epithelial cells. The results revealed the reversed effect of IL-17 on the impaired proliferative capacity of the alveolar epithelium induced by LCN2 overexpression, providing new clues for the treatment of lung injury diseases.