Objective To investigate the effects and underlying mechanisms of Shexiang Baoxin Pill (SBP) on valvular dysfunction in rats induced by wire injury. Methods A rat model of aortic valve injury was established using a standardized wire injury method. Animals were randomly divided into a control group, sham-operated group, model group, and SBP low-, medium-, and high-dose intervention groups. Aortic valve function was evaluated by echocardiography. Histopathological changes were assessed using hematoxylin-eosin (HE) and Masson's trichrome staining. Serum levels of lipid peroxides (LPO), malondialdehyde (MDA), superoxide dismutase (SOD), glutathione (GSH), and total iron were measured using biochemical assays. The expression levels of ferroptosis-related proteins (ACSL4, SLC7A11, GPX4) and osteogenic markers (RUNX2, BMP2) in valve tissues were detected by Western blotting and RT-qPCR. Results Compared to the model group, the SBP medium- and high-dose groups significantly increased the aortic valve orifice area (3.70±0.04 mm2 and 3.90±0.11 mm2 vs. 2.25±0.37 mm2, P<0.05), reduced the transvalvular pressure gradient (0.52±0.09 mmHg and 0.49±0.13 mmHg vs. 0.90±0.17 mmHg, P<0.05), and decreased the aortic valve peak flow velocity (68.83±4.98 cm/s and 63.61±11.43 cm/s vs. 87.14±11.22 cm/s, P<0.05). HE and Masson staining results demonstrated that SBP alleviated valve thickening and fibrosis (fibrotic area: 35.98±5.25% vs. 53.01±2.44%, P<0.05). Biochemical tests showed that SBP reduced serum levels of lipid peroxidation products (LPO and MDA) and total iron ions while increasing SOD and GSH levels (P<0.05). Western blot and RT-qPCR results indicated that SBP downregulated the expression of ferroptosis-related protein ACSL4 (P<0.05) while upregulating anti-ferroptosis proteins SLC7A11 and GPX4 (P<0.05) and inhibiting the expression of osteogenic molecules RUNX2 and BMP2 (P<0.05). Conclusion SBP may alleviate valve dysfunction induced by mechanical injury in rats by modulating oxidative stress and restoring iron homeostasis. These findings provide experimental evidence for the potential role of SBP in the early intervention of valvular disease. However, the precise active components, molecular targets, and clinical translation of SBP require further investigation.