Journal of ethnopharmacology · 2025
Magnoliae Officinalis Cortex volatile oil alleviated asthma via dual cAMP-mediated pathways: Anti-Inflammation and Bronchodilation.
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Li Kedi, Cao Zhangjing, Sun Jiayao, Liu Ruizhi, Wen Xinya, Tang Fei, Liu Lin, Peng Fu, Peng Cheng, Ao Hui
Аннотация
ETHNOPHARMACOLOGICAL RELEVANCE: Magnoliae Officinalis Cortex, a commonly used Chinese medicinal herb, has a long history in traditional East Asian medicine and is widely employed in the treatment of gastrointestinal disorders, asthma, depression, and other ailments. However, the potential of volatile oil derived from the bark of Magnolia officinalis Cortex (MVO) in asthma treatment remains to be determined.
AIM OF THE STUDY: This study aimed to explore the therapeutic effect of MVO on asthma and to explore its pathway and molecular mechanism under cAMP signal background.
METHODS: This study combined GC-MS with in vivo and in vitro experiments to elucidate the anti-asthmatic mechanism of MVO. An OVA-induced asthma model was established to evaluate the therapeutic effect of MVO via pulmonary function tests, H&E, BALF inflammatory cell counting, and ELISA. Fluo-4 AM, immunofluorescence and WB were further used to explore the underlying mechanism. In vitro, isolated tracheal rings were used as the object, and contraction models were constructed with KCl and acetylc holine to observe the relaxatory effect of MVO. Nifedipine (an L-type calcium channel blocker) and Pyr3 (a TRPC3 channel inhibitor) were used to intervene in the calcium signaling pathway, and the involvement of the cAMP pathway was analyzed by detecting cAMP level.
RESULTS: GC-MS analysis identified high concentrations of α-eudesmol, β-eudesmol, γ-eudesmol, and o-cymene in MVO. In vivo experiments showed that MVO reduced OVA-induced inflammatory cell infiltration and mucus secretion, improved pulmonary function, decreased Th2-type cytokines in BALF and serum IgE level, up-regulated the level of cAMP and the expressions of p-PKA/p-CREB in lung tissues, and inhibited NF-κB activation, reducing Ca2+ level and membrane localization in lung tissues. In vitro experiments showed that MVO could relax tracheal smooth muscle contractions induced by KCl and ACh in a dose-dependent manner. Application of nifedipine and Pyr3 confirmed that MVO exerted its relaxant effect by blocking L-VDCC and NSCC/TRPC channels.
CONCLUSION: MVO attenuated airway hyperresponsiveness by modulating the cAMP/PKA/CREB pathway, which subsequently suppressed NF-κB-driven inflammatory responses, while concurrently restoring cAMP/Ca2+ homeostasis. Significantly, our study demonstrated a novel dual-action therapeutic strategy targeting cAMP for asthma, bridging bronchodilatory and anti-inflammatory effects.
AIM OF THE STUDY: This study aimed to explore the therapeutic effect of MVO on asthma and to explore its pathway and molecular mechanism under cAMP signal background.
METHODS: This study combined GC-MS with in vivo and in vitro experiments to elucidate the anti-asthmatic mechanism of MVO. An OVA-induced asthma model was established to evaluate the therapeutic effect of MVO via pulmonary function tests, H&E, BALF inflammatory cell counting, and ELISA. Fluo-4 AM, immunofluorescence and WB were further used to explore the underlying mechanism. In vitro, isolated tracheal rings were used as the object, and contraction models were constructed with KCl and acetylc holine to observe the relaxatory effect of MVO. Nifedipine (an L-type calcium channel blocker) and Pyr3 (a TRPC3 channel inhibitor) were used to intervene in the calcium signaling pathway, and the involvement of the cAMP pathway was analyzed by detecting cAMP level.
RESULTS: GC-MS analysis identified high concentrations of α-eudesmol, β-eudesmol, γ-eudesmol, and o-cymene in MVO. In vivo experiments showed that MVO reduced OVA-induced inflammatory cell infiltration and mucus secretion, improved pulmonary function, decreased Th2-type cytokines in BALF and serum IgE level, up-regulated the level of cAMP and the expressions of p-PKA/p-CREB in lung tissues, and inhibited NF-κB activation, reducing Ca2+ level and membrane localization in lung tissues. In vitro experiments showed that MVO could relax tracheal smooth muscle contractions induced by KCl and ACh in a dose-dependent manner. Application of nifedipine and Pyr3 confirmed that MVO exerted its relaxant effect by blocking L-VDCC and NSCC/TRPC channels.
CONCLUSION: MVO attenuated airway hyperresponsiveness by modulating the cAMP/PKA/CREB pathway, which subsequently suppressed NF-κB-driven inflammatory responses, while concurrently restoring cAMP/Ca2+ homeostasis. Significantly, our study demonstrated a novel dual-action therapeutic strategy targeting cAMP for asthma, bridging bronchodilatory and anti-inflammatory effects.