Stellate ganglion irradiation alleviates airway inflammation in asthmatic mice via activating SIRT1 signaling pathway.

Asthma is a chronic inflammatory respiratory disease that seriously affects patients' quality of life. Although various pharmacological treatments are currently available, some patients still have poor responses, highlighting the urgent need for new intervention strategies. In recent years, stellate ganglion irradiation (SGI), as an emerging neuromodulation technique, has shown unique therapeutic advantages in various inflammatory diseases. However, the mechanism by which SGI alleviates asthma remains unclear. Silent information regulator 1 (SIRT1), an NAD+-dependent histone deacetylase, plays a key role in regulating cellular inflammatory responses by inhibiting NF-κB and other inflammatory signaling pathways. Given the involvement of SIRT1 and NF-κB imbalance in the pathogenesis of asthmatic airway inflammation, we hypothesize that SGI may alleviate asthmatic inflammation by activating SIRT1 and inhibiting NF-κB activation. To test this hypothesis, we used an ovalbumin (OVA)-induced mouse model of asthma to comprehensively evaluate the effects of SGI on asthma pathophysiology and explore the mediating role of the SIRT1-NF-κB pathway. We found that compared with the asthma group, SGI treatment significantly improved the general symptoms of mice, reduced airway hyperresponsiveness, alleviated inflammatory cell infiltration and cytokine levels in bronchoalveolar lavage fluid (BALF), and ameliorated lung histopathological changes. Mechanistic studies showed that SIRT1 expression was downregulated and the NF-κB pathway was activated in the lung tissues of asthmatic mice, while SGI treatment upregulated SIRT1 expression and inhibited NF-κB activity. In conclusion, this study reveals for the first time that SGI alleviates asthmatic airway inflammation through the SIRT1-NF-κB pathway, providing a new approach for the adjuvant treatment of asthma.