The present study aimed to investigate the regulatory effects and mechanisms of human placental extracts (HPE) on rats and cell models of ovalbumin (OVA)‑induced allergic rhinitis (AR). IFN‑y and LPS induced AR in vitro. A total of 32 male Sprague‑Dawley (SD) rats were randomly divided into the following four groups: Sham group, model group, model + HPE group and model + HPE + AMPK inhibitor group (n=8 rats/group). With the exception of the sham group, the remaining three groups were sensitized with OVA to establish an AR model, followed by various treatments. Hematoxylin and eosin staining was utilized to observe morphological changes in the nasal mucosa, ELISA was employed to measure serum levels of IL‑1β, interferon (IFN)β, immunoglobulin (Ig)E, IgG1 and IgG2a, and western blotting was conducted to assess protein expression across the groups. The sham group exhibited intact tissue structure with no notable pathological alterations. The model group demonstrated pronounced pathological features, including extensive infiltration of inflammatory cells, tissue shedding and edema. The model + HPE group revealed a gradual restoration of tissue architecture, characterized by reduced edema and inflammatory infiltration, whereas the model + HPE + AMPK inhibitor group again exhibited significant inflammatory cell infiltration and other pathological manifestations. Compared with the sham operation group, the levels of IL‑1β, IFNβ, IgE, IgG1 and IgG2a in the serum of the model group were elevated. The levels of IL‑1β, IFNβ, IgE, IgG1 and IgG2a in the model + HPE group were lower than those in the model group. In addition, the levels of IL‑1β, IFNβ, IgE, IgG1 and IgG2a in the model + HPE + AMPK inhibitor group were higher than those in the model + HPE group. Relative to the sham group, the expression levels of phosphorylated (p)‑AMPK/total (t)‑AMPK, p‑Src homology 2‑containing phosphatase (SHP)1/t‑SHP1 and p‑SHP2/t‑SHP2 were diminished, whereas the expression levels of p‑STING/t‑STING and p‑TBK1/t‑TBK1 were heightened in the model group. In comparison to the model group, the expression levels of p‑AMPK/t‑AMPK, p‑SHP1/t‑SHP1 and p‑SHP2/t‑SHP2 were enhanced, whereas the expression levels of p‑STING/t‑STING and p‑TBK1/t‑TBK1 were reduced in the model + HPE group. Conversely, when compared with the model + HPE group, the expression levels of p‑AMPK/t‑AMPK, p‑SHP1/t‑SHP1 and p‑SHP2/t‑SHP2 were decreased, whereas those of p‑STING/t‑STING and p‑TBK1/t‑TBK1 were increased in the model + HPE + AMPK inhibitor group. In conclusion, HPE may inhibit AR by modulating the AMPK/SHP1/SHP2/STING signaling pathway.