Objective To investigate the intervention effects of Brassica rapa L. (BR) extract on electrocardiographic parameters and myocardial tissue damage in hypobaric hypoxia-exposed mice, and explore its molecular regulatory mechanisms. Methods Sixty male SPF ICR mice (8 weeks old) were randomly divided into three groups: the normoxic BR, the hypobaric hypoxic BR, and the hypobaric hypoxic model groups. A 21-day hypobaric hypoxia mouse model was subsequently established. Cardiac electrophysiology, myocardial histopathology (H&E staining), and real-time quantitative PCR were applied to evaluate cardiac function, myocardial structural damage, and the expression patterns of antioxidant (Cat, Sod2), lipid metabolism (Plin5), and angiogenesis-related genes (Vegfa). Results The hypobaric hypoxic model group exhibited significant electrocardiographic abnormalities, including reduced QRS amplitude and elevated ST segments (P＜0.01 for both), accompanied by myocardial fiber disruption, nuclear pyknosis, and edema. BR intervention markedly alleviated these functional and structural impairments. Gene expression analysis revealed transient upregulation of Cat and Sod2 in the hypoxic BR group at day 1 of hypoxia exposure (P＜0.05), with later expression levels comparable to the normoxic BR group, while Cat and Sod2 in the hypobaric hypoxic model group remained downregulated at both 7 and 21 days (P＜0.05); Plin5 in the hypoxic BR group was rapidly upregulated at day 1 (P＜0.05) and returned to baseline levels by day 21, while remaining persistently downregulated in the model group (P＜0.05); Vegfa in the hypoxic BR group was significantly upregulated at day 1 (P＜0.05), markedly downregulated at day 7 and returned to baseline by day 21, while Vegfa expression in the model group remained persistently low throughout hypoxic exposure (P＜0.05), despite a transient increase at day 1 (P＜0.05).Conclusion BR alleviates hypobaric hypoxia-induced cardiac electrophysiological dysfunction and structural damage through time-dependent regulation of antioxidant, lipid metabolism, and angiogenesis-related genes. This protective mechanism involves coordinated early-phase stress responses and long-term homeostatic regulation, offering a potential therapeutic strategy for high-altitude hypoxia-induced cardiac injury