Luteolin inhibits autophagy in allergic asthma by activating PI3K/Akt/mTOR signaling and inhibiting Beclin-1-PI3KC3 complex

•OVA-induced inflammation activates autophagy in lung tissues of mice.•The autophagy level of lung tissues is positively correlated with eosinophils.•Luteolin inhibits inflammation while inhibiting autophagy.•Luteolin activates the PI3K/Akt/mTOR signaling pathway.•Luteolin inhibites the Beclin1-PI3K...

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Bibliographic Details
Published in:International immunopharmacology 2021-05, Vol.94, p.107460-107460, Article 107460
Main Authors: Wang, Shiyuan, Wuniqiemu, Tulake, Tang, Weifeng, Teng, Fangzhou, Bian, Qin, Yi, La, Qin, Jingjing, Zhu, Xueyi, Wei, Ying, Dong, Jingcheng
Format: Article
Language:English
Subjects:
1-Phosphatidylinositol 3-kinase
AKT protein
Allergens
Animal tissues
Animals
Anti-Asthmatic Agents - pharmacology
Anti-Asthmatic Agents - therapeutic use
Asthma
Asthma - drug therapy
Asthma - immunology
Autophagy
Autophagy - drug effects
Beclin-1 - immunology
Bronchoalveolar Lavage Fluid - cytology
Bronchoalveolar Lavage Fluid - immunology
Bronchus
Cell Line
Collagen
Cytokines - immunology
Female
Flavonoids
Hypersensitivity
Immunoglobulin E
Inflammation
Inflammatory diseases
Interleukin 13
Interleukin 5
Lungs
Luteolin
Luteolin - pharmacology
Luteolin - therapeutic use
Mice
Mice, Inbred BALB C
Mucus
Ovalbumin
Phagocytosis
Phosphatidylinositol 3-Kinases - immunology
PI3K signalings
Proto-Oncogene Proteins c-akt - immunology
Regulatory mechanisms (biology)
Respiratory tract
Respiratory tract diseases
Signal Transduction - drug effects
TOR protein
TOR Serine-Threonine Kinases - immunology
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Summary:•OVA-induced inflammation activates autophagy in lung tissues of mice.•The autophagy level of lung tissues is positively correlated with eosinophils.•Luteolin inhibits inflammation while inhibiting autophagy.•Luteolin activates the PI3K/Akt/mTOR signaling pathway.•Luteolin inhibites the Beclin1-PI3KC3 protein complex. Allergic asthma is a common chronic inflammatory disease characterized by airway inflammation, mucus hypersecretion and airway remodeling. Autophagy is a highly conserved intracellular degradation pathway in eukaryotic cells. There is growing evidence suggesting that dysregulation of autophagy is involved in the pathological process of asthma. Luteolin is a typical flavonoid compound with anti-inflammatory, anti-allergic and immune-enhancing functions. Previous studies have shown that luteolin can attenuate airway inflammation and hypersensitivity in asthma. However, whether luteolin can play a role in treating asthma by regulating autophagy remains unclear. The aim of the present study was to evaluate the therapeutic effect of luteolin on ovalbumin (OVA)-induced asthmatic mice, observe its effect on the level of autophagy in lung tissues, and further elucidate its underlying mechanism. The results showed that OVA-induced mice developed airway hyperresponsiveness, mucus over-production and collagen deposition. The number of inflammatory cells, levels of interleukin (IL)-4, IL-5 and IL-13 in bronchoalveolar lavage fluid (BALF) and OVA-specific IgE in serum were significantly increased. Furthermore, the infiltration of inflammatory cells was observed along with the activation of autophagy in lung tissues. Luteolin treatment significantly inhibited the OVA-induced inflammatory responses and the level of autophagy in lung tissues as well. Moreover, luteolin activated the PI3K/Akt/mTOR pathway and inhibited the Beclin-1-PI3KC3 protein complex in lung tissues of asthmatic mice. In conclusion, this study explored the regulatory mechanism of luteolin on autophagy in allergic asthma, providing biologic evidence for its clinical application.
ISSN:1567-5769
1878-1705
DOI:10.1016/j.intimp.2021.107460