Potential effect and mechanism of ultrashort wave therapy in mice with chronic rhinosinusitis
Year: 2026
Type: article
Abstract: Rhinosinusitis is an inflammatory condition that impacts both the nasal passages and the paranasal sinuses. Currently, there is no systematic or standardized treatment protocol for paediatric chronic rhinosinusitis (CRS). The aim of the present study was to conduct a preliminary investigation of the role and mechanism of ultrashort wave therapy in mice with CRS. Haematoxylin and eosin staining was performed to observe histopathological changes. Terminal deoxynucleotidyl transferase nick-end labelling assay was used to assess apoptosis in the sinus mucosa. Both immunofluorescence and enzyme-linked immunosorbent assay were performed to evaluate the expression levels of IFN-γ, IL-1α, TNF-α, and IL-10. Proteins associated with the p38/JNK/ERK signalling pathway were assessed using western blotting. The results revealed that ultrashort wave therapy significantly improved the histopathology of the sinus mucosa, particularly in maintaining the integrity of the ciliary structures. In addition, ultrashort wave therapy stimulated a notable decrease in apoptosis and inflammation in sinus mucosa samples. The phosphorylation levels of p38, JNK, and ERK were markedly inhibited in the sinus mucosa of mice with CRS subjected to ultrashort wave intervention. The findings of the present study elucidate a preliminary mechanism underlying the effects of ultrashort wave therapy on CRS progression. This suggests that ultrashort waves may be conducive to maintaining the integrity of the ciliary structures, inhibiting apoptosis, and reducing inflammation in the sinus mucosa. These effects are likely mediated through the inhibition of the p38/JNK/ERK signalling pathway.
Source: Biomedical Reports
DOI: 10.3892/br.2026.2109
Authors: Huifang Xu, Jing Weng, Quan Bao, Yuqiang Jiang, Cong Xiao, Liujun Chen
Language: English
Subfield: Otorhinolaryngology
Field: Medicine
Domain: Health Sciences
Open Access status: diamond
OpenAlex ID: W7124941971
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