Abstract:
OBJECTIVE To investigate the effects of the split formulas of Biyuan Heji (BYHJ) on paranasal sinus mucosal inflammation in rats with acute rhinosinusitis (ARS) based on the pathogenesis of "wind-cold transforming into lung-heat".
METHODS Unilateral nasal cavity occlusion combined with nasal dripping of Staphylococcus aureus were performed to establish a rat model of ARS. SD rats were randomly divided into blank, model, BYHJ (wind-cold removal + lung-heat removal), lung-heat removal, wind-cold removal, and positive drug groups, with 6 rats in each group. The rats were treated with the corresponding drugs for 7 d and then the samples were collected. HE staining was used to observe the pathological changes of rat paranasal sinus mucosa tissues, ELISA was employed to determine the levels of interleukin-1β (IL-1β), IL-6, IL-8, IL-9, IL-10, and IL-12 in serum, immunohistochemistry (IHC) was adopted to measure the protein expression of tumor necrosis factor-α (TNF-α) and intercellular adhesion molecule (ICAM-1) in paranasal sinus mucosa tissues, and Western blot was used to detect the protein expression of phosphorylated p38 mitogen-activated protein kinase (p38 MAPK), nuclear transcription factor-κB p50 (NF-κB p50), and NF-κB p65 in paranasal sinus mucosa tissues.
RESULTS The acute sinusitis rat inflammation model was successfully established. Compared with the model group, the water drinking, diet eating, and body weight of rats in the BYHJ group, wind-cold removal, lung-heat removal, and positive drug groups were significantly improved, the aggregation of inflammatory cells in the paranasal sinus mucosal tissue was reduced, and the levels of IL-1β, IL-6, IL-8, IL-9, and IL-12 in the serum were significantly reduced (P < 0.01), IL-10 content significantly increased (P < 0.01), the protein expression of TNF - α, ICAM-1, p38 MAPK, NF-κB p50, and NF-κB p65 in the paranasal sinus mucosa was significantly decreased (P < 0.01). The comparison between various traditional Chinese medicine groups showed that the decrease of IL-1β, IL-6, IL-8, IL-9, IL-12, TNF-α, ICAM-1, p38 MAPK, NF-κB p50, and NF-κB p65 and the increase of IL-10 in the BYHJ group were better than those in the split formula groups (P < 0.01), and the lung-heat removal group was better than the wind-cold removal group (P < 0.01).
CONCLUSION BYHJ and its split formulas can effectively inhibit the inflammatory response in rats with ARS.