Impact of <i>Lonicera japonica</i> 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. Purpose 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 &lt; .05). Treatment with LJE notably reduced symptom severity in the modeling group relative to the model control group ( p &lt; .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 &lt; .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 &lt; .05), while IL-4 and IL-10 levels were higher in the modeling group and control group compared to the model control group ( p &lt; .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.