Research Information System
RESPIRATORY PHYSIOLOGY & NEUROBIOLOGY, vol.339, 2026 (SCI-Expanded, Scopus)
Background: Asthma is a multifactorial chronic inflammatory airway disease affecting 5 % of children and 10 % of adults and there is no curative treatment. Recent studies have revealed that mitochondrial dysfunction is an important contributor to the pathophysiology of various respiratory diseases. Objectives: In this study, the effect of AP39, a mitochondria-targeted slow-releasing hydrogen sulfide (H2S) donor, was investigated in a mouse model of ovalbumin (OVA)-induced allergic asthma. Methods: Pulmonary function (airway resistance and dynamic compliance), inflammatory cells and cytokines in bronchoalveolar lavage (BAL) fluid, and histopathology of the lungs were evaluated in 8-12-week-old female C57BL/6 mice. Results: The OVA-induced allergic asthma model resulted in bronchial hyperreactivity, inflammatory cell infiltration in peribronchial and parenchymal areas in the lungs, increased Th2 cytokines and eosinophil numbers in BAL fluid. Treatment with AP39 (1000 nmol/kg) prevented bronchial hyperreactivity and suppressed the elevated IL-4, IL-5 and IL-13 cytokine levels, inhibited the increase of lymphocyte and eosinophil cells, and reduced histopathological changes in lung tissue. Treatment with a lower dose of AP39 (250 nmol/kg) had slightly less but still significant effects on bronchial hyperreactivity, inflammatory cells and histopathological changes, yet had no effect on cytokine levels. Conclusion: AP39 treatment prevented pathophysiological changes in allergic airway inflammation. Therefore, targeting the mitochondria with H2S donors may be a promising therapeutic potential in allergic respiratory diseases.