TLR4型
炎症
卵清蛋白
鼻粘膜
医学
NF-κB
免疫学
药理学
促炎细胞因子
汤剂
敏化
免疫系统
内科学
作者
Qi Yang,Yao Sun,J.G. An,Lirong Wang,Chengfei Zhang,Y. Fei,Kunmin Wu,Xiaofu Zhai,Yongjun Wu
摘要
Introduction: Allergic rhinitis (AR) is a systemic immune inflammatory response disease of the nasal mucosa. Current treatment strategies for AR are limited, owing to a lack of safety and the inability to cure the condition completely. Xiaoqinglong decoction (XQLD), a classical chinese medicine prescription, is widely used to treat AR with a good curative effect. Although the clinical effect of XQLD has been demonstrated, the molecular mechanisms of therapeutical effect were unclear. Hence, the study aimed to investigate effects of XQLD on inflammation and the underlying mechanism for AR management. Methods: Ovalbumin sensitization was used to induce AR in rats, and the nasal symptoms were evaluated. Hematoxylin-eosin staining was performed to detect epithelial cells of the nasal mucosa. Inflammatory factors were estimated to evaluate the anti-inflammatory effect of XQLD. Toll-like receptor 4 (TLR4) activity and myeloid differentiation factor 88 (MyD88)/nuclear factor kappa B (NF-κB) pathway were determined via immunofluorescence and Western blotting. Mitochondrial morphology and damage-related factors were assessed to determine the protective effect of XQLD. Results: The results showed that XQLD supplementation inhibited AR-induced release of inflammatory factors, relieved nasal symptoms, and improved mitochondrial functions. Moreover, it suppressed TLR4 and MyD88 expression as well as NF-κB p65 acetylation following AR. Conclusion: Inflammatory response and mitochondrial injury and the related MyD88/NF-κB signaling pathway play crucial roles in AR. XQLD supplementation inhibits AR-induced inflammation and mitochondrial injury by regulating TLR4 expression and TLR4-mediated MyD88/NF-κB pathway activation, thereby facilitating the therapeutic effect.
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