To explore whether oleuropein can mediate lipopolysaccharide-induced oxidative stress and apoptosis in alveolar epithelial cells induced by long non-coding ribonucleic acid Gm4419. Mouse alveolar type II epithelial cells were isolated and cultured, and divided into control, lipopolysaccharide, lipopolysaccharide+oleuropein, lipopolysaccharide+si-NC, lipopolysaccharide+si-Gm4419, lipopolysaccharide+oleuropein+plasmid cloning deoxyribonucleic acid, and lipopolysaccharide+oleuropein+plasmid cloning deoxyribonucleic acid Gm4419 groups. Determination of malondialdehyde content and superoxide dismutase activity in cells was undertaken using the indicated kits. Detection of apoptosis was done using flow cytometry. Protein levels were detected by Western blotting, and long non-coding ribonucleic acid Gm4419 expression was detected by reverse transcription quantitative polymerase chain reaction. Lipopolysaccharide stimulation elevated malondialdehyde content, reduced superoxide dismutase activity, and facilitated cell apoptosis in mouse alveolar type II epithelial cells. Furthermore, oleuropein treatment decreased lipopolysaccharide-induced oxidative stress and apoptosis in mouse alveolar type II epithelial cells. Moreover, lipopolysaccharide caused the upregulation of Gm4419 in mouse alveolar type II epithelial cells, and Gm4419 silencing weakened lipopolysaccharide-induced mouse alveolar type II epithelial cells oxidative stress and apoptosis. In addition, Gm4419 overexpression partly overturned oleuropein treatment-mediated effects on lipopolysaccharide induced mouse alveolar type II epithelial cells oxidative stress and apoptosis. Oleuropein may inhibit lipopolysaccharide induced alveolar epithelial cell oxidative stress and apoptosis by downregulating Gm4419.