Immunological investigations · 2026
Propofol Inhibits HIF-1α/NLRP3 Signaling Pathway and Mast Cell Activation to Ameliorate Airway Inflammation in Allergic Asthma.
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.
Zhang Yuzhu, Xia Jiangling, An Xiaona, Chen Luning, Chen Zhenzhen
Аннотация
BACKGROUND: The objective was to assess the effects of propofol on ovalbumin (OVA)-induced asthma in a mouse model and the efficacy of propofol in stabilizing mast cells and inhibiting the production of inflammatory mediators.
METHODS: Animal model of asthma induced by OVA was employed to evaluate the effect of propofol. Tissues from the lungs were retrieved for HE staining. The levels of IgE, IFN-γ, MPO, and so on was deteced. Bone marrow mast cells (BMMCs) were isolated to examine the suppressive action of propofol on the degranulation.
RESULTS: Propofol significantly reduced airway hyperresponsiveness and IgE, Th2 cytokines, and inflammatory cytokines in OVA-induced asthma model. Inhibited BMMCs degranulation and the production of inflammatory cytokines. Additionally, propofol inhibited the expression of HIF-1α and NLRP3 in asthma models. Overexpression HIF-1α in BMMCs reverses the effect of propofol. NLRP3 inhibition attenuates allergic asthma in DNP-HSA-treated DMMCs with or without overexpression HIF-1α. In terms of the mechanism, propofol interacts with HIF-1α directly, thereby disrupting HIF-1α-NLRP3 interaction and attenuating allergic asthma.
CONCLUSION: Propofol markedly improved OVA-induced asthma and inhibited mast cell degranulation by binding competitively to HIF-1α, thereby disrupting the HIF-1α-NLRP3 interaction and attenuating allergic asthma.
METHODS: Animal model of asthma induced by OVA was employed to evaluate the effect of propofol. Tissues from the lungs were retrieved for HE staining. The levels of IgE, IFN-γ, MPO, and so on was deteced. Bone marrow mast cells (BMMCs) were isolated to examine the suppressive action of propofol on the degranulation.
RESULTS: Propofol significantly reduced airway hyperresponsiveness and IgE, Th2 cytokines, and inflammatory cytokines in OVA-induced asthma model. Inhibited BMMCs degranulation and the production of inflammatory cytokines. Additionally, propofol inhibited the expression of HIF-1α and NLRP3 in asthma models. Overexpression HIF-1α in BMMCs reverses the effect of propofol. NLRP3 inhibition attenuates allergic asthma in DNP-HSA-treated DMMCs with or without overexpression HIF-1α. In terms of the mechanism, propofol interacts with HIF-1α directly, thereby disrupting HIF-1α-NLRP3 interaction and attenuating allergic asthma.
CONCLUSION: Propofol markedly improved OVA-induced asthma and inhibited mast cell degranulation by binding competitively to HIF-1α, thereby disrupting the HIF-1α-NLRP3 interaction and attenuating allergic asthma.