RT Journal T1 Baicalin Attenuates Allergic Rhinitis in Rats via Suppressing TLR4/AP-1 Inflammatory Signaling Pathway A1 Fengbo Yang A1 Fengjiao Li A1 Xing Chen A1 Ping Lv A1 Ruhui Xiao A1 Daxiong Ding A1 Qian Li JF Journal of Animal and Plant Sciences JO JAPS SN 1018-7081 VO 35 IS 5 SP 1291 OP 1301 YR 2025 FD 2025/09/30 DO DOI https://doi.org/10.36899/JAPS.2025.5.0110 AB

Allergic rhinitis (AR) is a type of non-infectious inflammatory disease of the nasal mucosa with a complex pathogenesis. This study investigated the mechanism of Baicalin (BAI, main active component of Radix Scutellariae extract) on the immune-inflammatory response in AR rat model through Toll-like receptor 4 (TLR4)/activator protein-1 (AP-1) pathway. Healthy male Sprague-Dawley (SD) rats were used as Control group. The AR model (AR group) was constructed by ovalbumin sensitization, and treated with 0.9 mg/kg loratadine (LRD group) and 20, 40, 80 mg/kg of BAI (LD-BAI group, MD-BAI group and HD-BAI group)via intragastric administration for 28 days. Symptom scores of the rats were assessed, peripheral blood was collected to determine Th1/Th2 cell ratios and changes ininflammatory cytokines, and nasal mucosa tissues were harvested to analyze pathological morphological changes and the expression of proteins related to the TLR4/AP-1 signaling pathway. As against Control group, AR group suggested increased symptom scores; nasal mucosa tissue edema, congestion, and inflammatory cell infiltration; decreased CD3+CD4+IFN-γ+Th1 proportion and increased CD3+CD4+IL-4+Th2 proportion in peripheral blood; elevated levels of inflammatory cytokinesIgE, IL-4, IL-17, and TNF-α, and decreased levels of IL-10 and IFN-γ; increased relative expression (RE) of TLR4, Ikkβ, NF-κB, p-JNK, and AP-1 proteins in nasal mucosa tissue (P≤0.05). As against AR group, LRD group, LD-BAI group, MD-BAI group, and HD-BAI group all suggested visible improvements in symptom scores, nasal mucosa tissue morphology, peripheral blood immune cell ratios, immune cytokine levels, and the expression of TLR4 pathway-related proteins in nasal mucosa, with HD-BAI group (80 mg/kg) demonstrating the most significant improvements in all indicators (P≤0.05vs. AR group). These findings suggest that BAI may alleviate AR symptoms by modulating immune-inflammatory responses via TLR4/AP-1 signaling. BAI can suppress the activation of TLR4 and its downstream Ikkβ/NF-κB, JNK/AP-1 inflammatory signaling pathwaysin AR rat model. BAI shows the developing novel treatment modalities for AR, warranting further investigation.

K1 Allergic rhinitis; Baicalin; nasal mucosa;inflammatory cytokines; TLR4; Ikkβ/NF-κB; JNK/AP-1 PB Pakistan Agricultural Scientists Forum LK https://thejaps.org.pk/AbstractView.aspx?mid=2025-JAPS-196