Immunity, inflammation and disease · 2026
Mometasone Furoate Alleviates PM2.5-Induced Pyroptosis of Nasal Mucosa Cells via Blocking JAK2/STAT3/AIM2 Inflammasome.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Shi Bin, Liu Zhiqi, Le Ge
Аннотация
OBJECTIVE: Mometasone furoate (MF) is a widely used intranasal corticosteroid for the management of allergic and non-allergic rhinitis. Recent evidence suggests that its therapeutic efficacy may involve mechanisms beyond traditional anti-inflammatory actions, including modulation of death in nasal mucosa cells. This study aimed to investigate the therapeutic effects of MF on chronic rhinitis, elucidates the underlying molecular mechanisms, and explores its clinical implications in rhinitis management.
METHODS: Enzyme-linked immunosorbent assay was used to detect cytokine release. Reverse transcription quantitative PCR was applied for detecting mRNA expression. Immunofluorescence was used detect LC3 expression. Protein express was detected using Western blot. Lactate dehydrogenase leakage assay was used to detect cytotoxicity. Terminal deoxynucleotidyl transferase dUTP nick-end labeling assay was used to detect death of nasal mucosa cells (NMCs). Luciferase and chromatin immunoprecipitation assays were used to verify the interaction between signal transducer and activator of transcription 3 (STAT3) and absent in melanoma 2 (AIM2).
RESULTS: MF significantly suppressed inflammatory response induced by PM2.5. MF suppressed PM2.5-induced cytotoxicity and pyroptosis of NMCs. Moreover, MF promotes the activation of autophagy. Mechanically, MF inhibited PM2.5-induced activation of Janus kinase 2/STAT3 signaling. STAT3 transcriptionally upregulated AIM2. The activation of AIM2 inflammasome attenuated the effects of MF and promoted the inflammation and pyroptosis of NMCs as well as suppressed the activation of autophagy.
CONCLUSION: In summary, MF protects against chronic rhinitis via suppressing AIM2-dependent pyroptosis of NMCs. Therefore, MF can be a therapeutic strategy for chronic rhinitis.
METHODS: Enzyme-linked immunosorbent assay was used to detect cytokine release. Reverse transcription quantitative PCR was applied for detecting mRNA expression. Immunofluorescence was used detect LC3 expression. Protein express was detected using Western blot. Lactate dehydrogenase leakage assay was used to detect cytotoxicity. Terminal deoxynucleotidyl transferase dUTP nick-end labeling assay was used to detect death of nasal mucosa cells (NMCs). Luciferase and chromatin immunoprecipitation assays were used to verify the interaction between signal transducer and activator of transcription 3 (STAT3) and absent in melanoma 2 (AIM2).
RESULTS: MF significantly suppressed inflammatory response induced by PM2.5. MF suppressed PM2.5-induced cytotoxicity and pyroptosis of NMCs. Moreover, MF promotes the activation of autophagy. Mechanically, MF inhibited PM2.5-induced activation of Janus kinase 2/STAT3 signaling. STAT3 transcriptionally upregulated AIM2. The activation of AIM2 inflammasome attenuated the effects of MF and promoted the inflammation and pyroptosis of NMCs as well as suppressed the activation of autophagy.
CONCLUSION: In summary, MF protects against chronic rhinitis via suppressing AIM2-dependent pyroptosis of NMCs. Therefore, MF can be a therapeutic strategy for chronic rhinitis.