<p>Oculomotor nerve injury impairs eye movement and pupil control. Intraorbital electroacupuncture (IEA) is a promising treatment, but its mechanisms remain unclear. This study investigates whether IEA promotes nerve recovery by inducing M2 macrophage polarization through the JAK1/STAT6 pathway. Sprague–Dawley (SD) rats with oculomotor nerve injury were divided into four groups: sham, control, IEA, and IEA + AS1517499 (JAK1/STAT6 inhibitor). Pupil diameter and abduction deviation were measured. Nerve structure was assessed with Luxol fast blue and Nissl staining. Western blotting analyzed JAK1/STAT6 pathway activation, and immunofluorescence quantified M1/M2 macrophages. The IEA group showed significant functional recovery in the oculomotor nerve, as evidenced by improvements in pupil diameter and abduction deviation compared to the control group. Histological analysis revealed better preservation of nerve structure in the IEA group, with reduced signs of damage. Western blot results demonstrated increased phosphorylation of STAT6 in the IEA group, indicating activation of the JAK1/STAT6 pathway. Immunofluorescence double staining revealed a higher ratio of M2 (CD206+, CD163+) macrophages relative to M1(CD86+ , iNOS+) macrophages in the IEA group. This effect was diminished in the IEA + AS1517499 group, suggesting that the therapeutic benefits of IEA are mediated through the JAK1/STAT6 pathway and M2 macrophage polarization. IEA promotes oculomotor nerve repair by inducing M2 macrophage polarization via the JAK1/STAT6 pathway, offering a potential therapeutic strategy for nerve injury.</p>