ArticleInternational journal of chronic obstructive pulmonary disease2016
The inhibitory mechanism of Cordyceps sinensis on cigarette smoke extract-induced senescence in human bronchial epithelial cells.
Article in International journal of chronic obstructive pulmonary disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 38 citations in OpenAlex.
- Research on the Mechanism of Natural Products Acting on Chronic Obstructive Pulmonary Disease.Food science & nutrition · 2026Review
- Multi-pathway targeting by natural products in chronic respiratory diseases: Opportunities, challenges, and future perspectives.Chinese herbal medicines · 2026Article
- Wnt signaling pathway in lung aging and aging-related chronic lung diseases.Biogerontology · 2025Review
- Cordyceps sinensis (CS) Alleviates Chronic Obstructive Pulmonary Disease Symptoms (COPD) by Targeting Inflammation, Apoptosis, and Oxidative Stress Through Ingredient-Gene-Disease Interaction.Immunity, inflammation and disease · 2025Article
- Exploring the mechanism of guben kechuan granules in the treatment of COPD via network pharmacology, molecular docking and molecular dynamics simulations.Scientific reports · 2025Article
- The GenusLife (Basel, Switzerland) · 2025Review
- Zerumbone liquid crystalline nanoparticles protect against oxidative stress, inflammation and senescence induced by cigarette smoke extract in vitro.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Natural Modulators of Key Signaling Pathways in Skin Inflammageing.Clinical, cosmetic and investigational dermatology · 2024Review
- Chemical components in cultivatedChinese herbal medicines · 2024Article
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- Attenuation of Cigarette-Smoke-Induced Oxidative Stress, Senescence, and Inflammation by Berberine-Loaded Liquid Crystalline Nanoparticles: In Vitro Study in 16HBE and RAW264.7 Cells.Antioxidants (Basel, Switzerland) · 2022Article
- The role of miRNAs in alveolar epithelial cells in emphysema.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2021Review
- Review
- The Protective Role of Bioactive Quinones in Stress-induced Senescence Phenotype of Endothelial Cells Exposed to Cigarette Smoke Extract.Antioxidants (Basel, Switzerland) · 2020Article
- Targeting p16-induced senescence prevents cigarette smoke-induced emphysema by promoting IGF1/Akt1 signaling in mice.Communications biology · 2019Article
- Article
- Nucleosides isolated fromInternational journal of chronic obstructive pulmonary disease · 2018Article
- The Function ofCanadian respiratory journal · 2018Article
- Modulation of NF-κB, MMP-1, and HAase byAvicenna journal of medical biotechnologyArticle
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesCellular senescence is a state of irreversible growth arrest induced either by telomere shortening (replicative senescence) or stress. The bronchial epithelial cell is often injured by inhaled toxic substances, such as cigarette smoke. In the present study, we investigated whether exposure to cigarette smoke extract (CSE) induces senescence of bronchial epithelial cells; and Cordyceps sinensis mechanism of inhibition of CSE-induced cellular senescence.
methodsHuman bronchial epithelial cells (16HBE cells) cultured in vitro were treated with CSE and/or C. sinensis. p16, p21, and senescence-associated-galactosidase activity were used to detect cellular senescence with immunofluorescence, quantitative polymerase chain reaction, and Western blotting. Reactive oxygen species (ROS), PI3K/AKT/mTOR and their phosphorylated proteins were examined to testify the activation of signaling pathway by ROS fluorescent staining and Western blotting. Then, inhibitors of ROS and PI3K were used to further confirm the function of this pathway.
resultsCellular senescence was upregulated by CSE treatment, and C. sinensis can decrease CSE-induced cellular senescence. Activation of ROS/PI3K/AKT/mTOR signaling pathway was enhanced by CSE treatment, and decreased when C. sinensis was added. Blocking ROS/PI3K/AKT/mTOR signaling pathway can attenuate CSE-induced cellular senescence.
conclusionCSE can induce cellular senescence in human bronchial epithelial cells, and ROS/PI3K/AKT/mTOR signaling pathway may play an important role in this process. C. sinensis can inhibit the CSE-induced senescence.
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