Impact of Lonicera japonica Extract on Nerve Growth Factor and Inflammatory Pathways in a Mouse Modeling of Allergic Rhinitis

Background: Although Lonicera japonica extract (LJE) has been widely used in traditional medicine for treating conditions such as heat-clearing, detoxification, and anti-bacterial purposes, its specific effects on allergic rhinitis (AR) remain underexplored. Objectives: This study aimed to elucidate how LJE influences nerve growth factor (NGF) levels and associated inflammatory pathways in AR modeling of mice. Materials and Methods: Chlorogenic acid, a key component of LJE, was isolated and optimized using orthogonal experiments and chromatographic techniques. An AR mouse modeling was established and divided into three groups: control group (no treatment), modeling group (LJE intervention), and modeling control group (model control group, saline intervention). Post-intervention, AR symptoms were evaluated, and serum and nasal mucosa tissues were analyzed. Western blotting was used to measure levels of PI3K, AKT, and NF-κB p65 proteins. At the same time, enzyme-linked immunosorbent assays (ELISA) quantified NGF, tumor necrosis factor (TNF)-α, interferon (IFN)-γ, interleukin (IL)-4, and IL-10 in serum and nasal mucosal tissue. Results: Chlorogenic acid was successfully extracted with optimal conditions being 70% ethanol, pH 5, a solvent-to-material ratio of 10:1, and an extraction time of 1.5 h. The AR symptoms in the modeling group and model control group were significantly more severe compared to the control group (p < .05). Treatment with LJE notably reduced symptom severity in the modeling group relative to the model control group (p < .05). Additionally, the levels of PI3K, AKT, and NF-κB p65 in nasal mucosal tissue of the modeling group were comparable to those in the control group and lower than in the model control group (p < .05). NGF, TNF-α, and IFN-γ levels in the modeling group and control group were significantly lower than those in the model control group (p < .05), while IL-4 and IL-10 levels were higher in the modeling group and control group compared to the model control group (p < .05). Conclusion: LJE effectively reduced NGF expression and alleviated AR symptoms in a mouse model, potentially through regulation of PI3K/Akt and NF-κB signaling pathways. This highlights LJE’s therapeutic potential for managing AR-related inflammation.