Purpose: To investigate the effect of miR-155 on allergic conjunctivitis (AC) in mice, and to elucidate the mechanism of action. Methods: Sixty (60) Balb/c mice were randomly divided into three groups with 20 mice per group. Ovalbumin (OVA) was used to induce experimental model of AC in mice. Mice in the AC+miR-155 siRNA group were given miR-SiRNA once daily for 2 weeks before inducing AC. The expressions of miR-155 in conjunctival tissue of the control and AC groups were assayed with reverse transcriptionpolymerase chain reaction (RT-PCR). In addition, anti-OVA IgE antibody, eotaxin, IL-13 and IFN-gamma levels were determined using ELISA (enzyme-linked immunosorbent assay). The regulatory effect of miR-155 on the NF-kappa B signal pathway in mice conjunctiva tissue with AC was determined using immunoblotting. Results: Higher miR-155 expression was seen in serum of AC group than in that of control group (p < 0.05). Inhibition of miR-155 mitigated AC-induced pathological injury, reduced infiltration of eosinophils, lowered serum levels of anti-AVO IgE antibody eotaxin and Il-13, and increased IFN-gamma level (p < 0.05). Phosphorylation of P65 of conjunctiva tissue of AC mice was blocked after inhibition of miR-155. Conclusion: The inhibition of miR-155 ameliorates AC in mice most likely via a mechanism related to the inhibition of phosphorylation of P65. This provides a theoretical basis for new drug research and development.