Discovery medicine · 2025
Amygdalin Alleviates Airway Inflammation and Remodeling in Asthma Mice: Involvement of TGF-β1/Smads Signaling Pathway.
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Zhao Jing, Wang Yamei, Wang Haixu
Аннотация
BACKGROUND: Asthma is a common respiratory system disease characterized by airway inflammation and airway remodeling. Amygdalin, an active component of the traditional Chinese medicine Bitter Almonds, has been shown to inhibit liver fibrosis via the inactivation of the transforming growth factor-beta 1 (TGF-β1)/Smads pathway. This study aims to investigate the effects of Amygdalin on airway inflammation and remodeling in asthma, as well as its regulatory mechanisms.
METHODS: An asthma mouse model was constructed using ovalbumin (OVA) induction. Mouse bronchoalveolar lavage fluid (BALF) and lung tissue were harvested for in vivo experiments, and airway smooth muscle cells (ASMCs) were isolated from BALB/c mice for in vitro experiments. The mechanism of Amygdalin and the TGF-β1/Smads signaling pathway in the mouse model was analyzed pathologically and molecularly using hematoxylin-eosin (HE) staining, Masson trichrome staining, Western blot, and enzyme-linked immunosorbent assay (ELISA).
RESULTS: Amygdalin ameliorated the pathological abnormalities of lung tissues in the OVA-induced mouse model, reducing inflammation by downregulating OVA-specific immunoglobulin E (IgE) and inflammatory factors interleukin (IL)-4, IL-5, and IL-13 (p < 0.001). It also reduced lung tissue fibrosis (p < 0.01). Additionally, Amygdalin inhibited the levels of TGF-β1, p-Smad2, and p-Smad3 proteins (p < 0.05), and downregulated the fibrosis markers alpha-smooth muscle actin (α-SMA), Collagen I, and Collagen III expression in the OVA-induced asthma mouse model (p < 0.01).
CONCLUSION: Amygdalin can regulate the TGF-β1/Smads signaling pathway and alleviate airway inflammation and remodeling in an asthma model in mice.
METHODS: An asthma mouse model was constructed using ovalbumin (OVA) induction. Mouse bronchoalveolar lavage fluid (BALF) and lung tissue were harvested for in vivo experiments, and airway smooth muscle cells (ASMCs) were isolated from BALB/c mice for in vitro experiments. The mechanism of Amygdalin and the TGF-β1/Smads signaling pathway in the mouse model was analyzed pathologically and molecularly using hematoxylin-eosin (HE) staining, Masson trichrome staining, Western blot, and enzyme-linked immunosorbent assay (ELISA).
RESULTS: Amygdalin ameliorated the pathological abnormalities of lung tissues in the OVA-induced mouse model, reducing inflammation by downregulating OVA-specific immunoglobulin E (IgE) and inflammatory factors interleukin (IL)-4, IL-5, and IL-13 (p < 0.001). It also reduced lung tissue fibrosis (p < 0.01). Additionally, Amygdalin inhibited the levels of TGF-β1, p-Smad2, and p-Smad3 proteins (p < 0.05), and downregulated the fibrosis markers alpha-smooth muscle actin (α-SMA), Collagen I, and Collagen III expression in the OVA-induced asthma mouse model (p < 0.01).
CONCLUSION: Amygdalin can regulate the TGF-β1/Smads signaling pathway and alleviate airway inflammation and remodeling in an asthma model in mice.