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Sophora flavescens Aiton alleviates particulate matter-exacerbated asthma through modulation of ROS/ MAPK/autophagy
Hoyeon Park1, Eom Ji Kim1, Eun-Young Kim1
1Department of Anatomy, College of Korean Medicine, Kyung Hee University, 26, Kyungheedae-ro, Dongdaemun-gu, Seoul, 02447, Republic of Korea.
Ethnopharmacological Relevance:
Sophora flavescens Aiton (SFA) has traditionally been used in East Asian medicine for its fever-reducing and dampness-drying properties. It is prescribed for the treatment of fever, skin eczema, asthma, and various inflammatory disorders. Building on these traditional applications, recent studies have reported its anti-asthmatic, anti-inflammatory, and antitumor activities. However, its mechanism of action against asthma exacerbated by particulate matter (PM) remains unclear.
Aim Of The Study:
In this study, we aimed to investigate the anti-inflammatory and anti-asthmatic effects of SFA by assessing its therapeutic efficacy, reactive oxygen species (ROS)-related pathways, and inflammatory biomarkers in a PM-exacerbated asthma model.
Materials And Methods:
In vitro, BEAS-2B cells were exposed to tumor necrosis factor-α and interleukin-4 in combination with PM to evaluate the effects of SFA on ROS generation, inflammation, and related signaling pathways. In vivo PM-exacerbated asthma model was established using ovalbumin-sensitized Balb/c mice, and the therapeutic effects of SFA were evaluated by analyzing inflammatory markers and histopathological changes.
Results:
SFA significantly reduced oxidative stress and pro-inflammatory cytokines. It also inhibited the phosphorylation of c-Jun N-terminal kinase and AKT, as well as Light chain 3 (LC3) expression, indicating regulation of inflammatory and autophagy-related pathways. In vivo, SFA decreased serum IgE levels, suppressed pro-inflammatory cytokine expression in lung tissue by modulating MAPK signaling, and significantly reduced airway smooth muscle thickness and LC3 II-positive areas.
Conclusion:
These findings suggest that SFA may effectively ameliorate PM-induced asthma exacerbation by inhibiting ROS production, modulating the MAPK/autophagy responses, and improving histopathological features.
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