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General Physiology and Biophysics 2020 General Physiology and Biophysics Vol.39, No.3, p.293–300, 2020
General Physiology and Biophysics 2020 General Physiology and Biophysics Vol.39, No.3, p.293–300, 2020
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General Physiology and Biophysics Vol.39, No.3, p.293–300, 2020 |
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| Title: Dexmedetomidine alleviates smoke-induced bronchial and alveolar epithelial cell injury | ||
| Author: Jiageng Hong, Qumin Chen, Yanbin Wang, Shaoli Lin, Guoqiang Su | ||
| Abstract: Dexmedetomidine (Dex) is a selective α2-adrenoceptor agonist and has ability to prevent inflammation and apoptosis in tissues injury. However, whether Dex could alleviate smoke-induced lung injury remains unknown. This study aimed to explore the protective effects of Dex against smoke-induced lung injury. Bronchial and alveolar epithelial cells were treated with cigarette smoke extract (CSE) for 24 h to simulate cigarette smoke-induced lung injury. Results showed that CSE reduced cell viability and increased levels of pro-inflammatory cytokines TNF-α, IL-1β and IL-6, thus activating NF-κB and COX2 expression. CSE also increased ROS generation, whereas lessened MnSOD and catalase generation. Besides, the ratio of apoptotic cells was enhanced upon CSE stimuli, together with disturbance of apoptotic-related proteins including Bcl-2, Bax and caspase-3. However, Dex reduced the damage of CSE to cell viability. The increased activities of TNF-α, IL-1β and IL-6 induced by CSE were partially attenuated by Dex. Dex also recovered the levels of NF-κB and COX2, as well as mnSOD, catalase and ROS. Furthermore, the increase of cell apoptosis together with imbalance of apoptotic proteins induced by CSE was rescued by Dex. Our results demonstrated that Dex alleviated CSE-induced lung injury through inhibition of inflammation, oxidative stress and apoptosis. |
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| Keywords: Apoptosis, Dexmedetomidine, Inflammation, Lung injury, Smoking | ||
| Published online: 10-Jun-2020 | ||
| Year: 2020, Volume: 39, Issue: 3 | Page From: 293, Page To: 300 | |
| doi:10.4149/gpb_2020003 |
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