Chinese Medicine in Regulating Signaling Pathways Related to Allergic Rhinitis： A Review / 中国实验方剂学杂志

ABSTRACT

Allergic rhinitis （AR）， a common disease in otolaryngology， is intractable with prolonged attack and greatly affects the daily life of patients. Western medicine adopts many therapeutic protocols， such as medication， immunotherapy， and surgery， and also shows disadvantages， including severe side effects and poor long-term curative effect. As reported by modern research， Chinese medicine has the characteristics of good safety， stable curative effect， multi-target and overall regulation， and has unique advantages in the prevention and treatment of AR. With the increasing clinical practice of Chinese medicine in the treatment of AR， scholars have carried out substantial basic research on the regulation of AR signaling pathways by monomers and Chinese medicinal compounds from molecule-cell-biology. To further explain the transduction mechanism of AR signaling pathways， this paper systematically summarized the research progress based on the studies of monomers and Chinese medicinal compounds to provide references for the in-depth research on the intervention of related signaling pathways by Chinese medicine. The conclusions were drawn as follows. The main signaling pathways involved included nuclear factor-kappa B （NF-κB） signaling pathway， TLR signaling pathway， interleukin （IL）-33/growth stimulation expressed gene 2 （ST2） signaling pathway， phosphoinositide 3-kinase/protein kinase B （PI3K/Akt） pathway， and mitogen-activated protein kinase （MAPK） pathway. As revealed， the signaling pathways involved in the treatment of AR by Chinese medicine interacted with each other and genes were not independent in exerting the effects. For example， TLR， as the upstream signal， affected the PI3K/Akt and MAPK signaling pathways， and NF-κB was the downstream substrate of PI3K/Akt， TLR， IL-33/ST2， and MAPK signaling pathways. It was found that IL-33/ST2， as a new signaling pathway， was correlated with the severity and prognosis of AR.