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      <ref-type name="Journal Article">17</ref-type>
      <contributors>
        <authors>
          <author>Fengbo Yang</author>
          <author>Fengjiao Li</author>
          <author>Xing Chen</author>
          <author>Ping Lv</author>
          <author>Ruhui Xiao</author>
          <author>Daxiong Ding</author>
          <author>Qian Li</author>
        </authors>
      </contributors>
      <titles>
        <title>Baicalin Attenuates Allergic Rhinitis in Rats via Suppressing TLR4/AP-1 Inflammatory Signaling Pathway</title>
        <secondary-title>Journal of Animal and Plant Sciences</secondary-title>
        <alt-title>JAPS</alt-title>
      </titles>
      <dates><year>2025</year><pub-dates><date>2025/09/30</date></pub-dates></dates>
      <volume>35</volume>
      <number>5</number>
      <pages>1291-1301</pages>
      <isbn>1018-7081</isbn>
      <electronic-resource-num>https://doi.org/10.36899/JAPS.2025.5.0110</electronic-resource-num>
      <abstract>&lt;p&gt;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&amp;nbsp;&lt;em&gt;Radix Scutellariae&amp;nbsp;&lt;/em&gt;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&lt;sup&gt;+&lt;/sup&gt;CD4&lt;sup&gt;+&lt;/sup&gt;IFN-&amp;gamma;&lt;sup&gt;+&lt;/sup&gt;Th1 proportion and increased CD3&lt;sup&gt;+&lt;/sup&gt;CD4&lt;sup&gt;+&lt;/sup&gt;IL-4&lt;sup&gt;+&lt;/sup&gt;Th2 proportion in peripheral blood; elevated levels of inflammatory cytokinesIgE, IL-4, IL-17, and TNF-&amp;alpha;, and decreased levels of IL-10 and IFN-&amp;gamma;; increased relative expression (RE) of TLR4, Ikk&amp;beta;, NF-&amp;kappa;B, p-JNK, and AP-1 proteins in nasal mucosa tissue (&lt;em&gt;P&amp;le;&lt;/em&gt;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 (&lt;em&gt;P&amp;le;0.05&lt;/em&gt;vs. 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 Ikk&amp;beta;/NF-&amp;kappa;B, JNK/AP-1 inflammatory signaling pathwaysin AR rat model. BAI shows the developing novel treatment modalities for AR, warranting further investigation.&lt;/p&gt;</abstract>
      <keywords><keyword>Allergic rhinitis; Baicalin; nasal mucosa;inflammatory cytokines; TLR4; Ikkβ/NF-κB; JNK/AP-1</keyword></keywords>
      <publisher>Pakistan Agricultural Scientists Forum</publisher>
      <urls><related-urls><url>https://thejaps.org.pk/AbstractView.aspx?mid=2025-JAPS-196</url></related-urls></urls>
    </record>
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