Abstract: Objective To explore the potential protective mechanism of malvidin in lipopolysaccharide (LPS)-induced septic acute lung injury (ALI).Methods A total of 30 male C57BL/6 mice were randomly divided into five groups (n=6): a control group, a LPS (10 mg/kg) group, and malvidin (5, 10, 20 mg/kg) + LPS groups. A mouse model of LPS-induced septic ALI was established. Hematoxylin-eosin staining was used to assess lung injury in the mice. Real-time quantitative PCR, biochemical assay kits, TUNEL staining, and transmission electron microscopy (TEM) were used to evaluate inflammatory response, oxidative stress, and apoptosis, respectirely.Results The LPS-induced septic ALI mouse model was successfully established. Compared with mice in the LPS group, those treated with malvidin showed significantly reduced lung swelling and alleviated inflammatory cell infiltration in lung tissues. The protein content in bronchoalveolar lavage fluid significantly decreased (P<0.05). The mRNA levels of pro-inflammatory factors interleukin-6 (IL-6), IL-1β, tumor necrosis factor-α(TNF-α), and inducible nitric oxide synthase (iNOS) in lung tissues significantly decreased, while the mRNA levels of the anti-inflammatory factor IL-10 significantly increased (P<0.001). The activities of antioxidant enzymes catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) were significantly enhanced (P<0.05), while the content of the oxidative product malondialdehyde (MDA) was significantly reduced (P<0.001). Apoptotic body formation in the tissue was inhibited, and the number of TUNEL-positive cells was reduced.Conclusions Malvidin has protective effect on LPS-induced septic ALI. Its mechanism involves inhibiting the inflammatory response, alleviating oxidative stress, and improving apoptosis, thereby restoring abnormal lung tissue morphology and maintaining bronchoalveolar integrity.