Journal of ethnopharmacology · 2025
Sophora flavescens Aiton alleviates particulate matter-exacerbated asthma through modulation of ROS/ MAPK/autophagy responses.
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.
Park Hoyeon, Kim Eom Ji, Kim Eun-Young, Son Dongbin, Joo Byung Duk, Kim Sangwoo, Sohn Youngjoo, Jung Hyuk-Sang
Аннотация
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.
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.