Zhao Kaixuan, Zhang Haoyue, Liu Yanbo, Zhou Ying, Zhi Juan, Wang Qianyu, Yang Dong
Department of Anesthesiology, Plastic Surgery Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Shijingshan District, Beijing, 100144, China.
Sci Rep. 2025 Aug 1;15(1):28092. doi: 10.1038/s41598-025-12901-y.
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.
哮喘是一种慢性炎症性呼吸系统疾病，严重影响患者的生活质量。尽管目前有各种药物治疗方法，但一些患者的反应仍然不佳，这凸显了对新干预策略的迫切需求。近年来，星状神经节照射（SGI）作为一种新兴的神经调节技术，在各种炎症性疾病中显示出独特的治疗优势。然而，SGI缓解哮喘的机制仍不清楚。沉默信息调节因子1（SIRT1）是一种依赖NAD+的组蛋白脱乙酰酶，通过抑制NF-κB和其他炎症信号通路在调节细胞炎症反应中起关键作用。鉴于SIRT1和NF-κB失衡参与哮喘气道炎症的发病机制，我们假设SGI可能通过激活SIRT1和抑制NF-κB激活来缓解哮喘炎症。为了验证这一假设，我们使用卵清蛋白（OVA）诱导的小鼠哮喘模型全面评估SGI对哮喘病理生理学的影响，并探讨SIRT1-NF-κB途径的介导作用。我们发现，与哮喘组相比，SGI治疗显著改善了小鼠的一般症状，降低了气道高反应性，减轻了支气管肺泡灌洗液（BALF）中的炎症细胞浸润和细胞因子水平，并改善了肺组织病理学变化。机制研究表明，哮喘小鼠肺组织中SIRT1表达下调，NF-κB途径激活，而SGI治疗上调SIRT1表达并抑制NF-κB活性。总之，本研究首次揭示SGI通过SIRT1-NF-κB途径缓解哮喘气道炎症，为哮喘的辅助治疗提供了新方法。
