Format

Send to

Choose Destination
Int J Chron Obstruct Pulmon Dis. 2016 Jul 28;11:1721-31. doi: 10.2147/COPD.S107396. eCollection 2016.

The inhibitory mechanism of Cordyceps sinensis on cigarette smoke extract-induced senescence in human bronchial epithelial cells.

Author information

1
Department of Pulmonary Diseases, Qilu Hospital, Shandong University, Jinan, Shandong, People's Republic of China; Department of Pulmonary Diseases, Weihai Municipal Hospital, Weihai, Shandong, People's Republic of China.
2
Department of Pulmonary Diseases, Qilu Hospital, Shandong University, Jinan, Shandong, People's Republic of China.
3
Department of Pulmonary Diseases, Weihai Municipal Hospital, Weihai, Shandong, People's Republic of China.
4
Institute of Biochemistry and Molecular Biology, School of Medicine, Shandong University, Jinan, Shandong, People's Republic of China.

Abstract

OBJECTIVES:

Cellular 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.

METHODS:

Human 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.

RESULTS:

Cellular 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.

CONCLUSION:

CSE 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.

KEYWORDS:

COPD; Cordyceps sinensis; ROS/PI3K/AKT/mTOR signaling pathway; senescence

PMID:
27555762
PMCID:
PMC4968689
DOI:
10.2147/COPD.S107396
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Dove Medical Press Icon for PubMed Central
Loading ...
Support Center