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Cigarette Smoke Exposure in Mice using a Whole-Body Inhalation System
Published on: October 22, 2020
The miR-146a/IGSF11 Axis Potentially Mediates the Protective Effect of Dexmedetomidine Against Cigarette
Xiao Chen1, Dan Wang1, Jing Du2
1Department of Anesthesiology, Hainan Affiliated Hospital of Hainan Medical University (Hainan General Hospital), Haikou, China, hainmc.edu.cn.
Background:
This study comprehensively examined the mechanism of the roles of dexmedetomidine (Dex) and miR-146a in chronic obstructive pulmonary disease (COPD).
Methods:
COPD models were established employing cigarette smoke extract (CSE)-exposed airway epithelium cell 16HBE and cigarette smoke-treated Sprague-Dawley rats, followed by interference with Dex and transfection. CCK-8 and flow cytometry assays were employed for the detection of cell viability and apoptosis. Further, the levels of factors related to the NF-κB pathway, inflammation, and apoptosis were measured by ELISA, qRT-PCR, and Western blot.
Results:
Dex and miR-146a mimic notably inhibited the inflammation and apoptosis of CSE-induced 16HBE cells via modulating the levels of TNF-α, IL-6, IL-8 (inflammatory cytokines), and caspase-3, Bcl-2, and Bax (apoptosis-associated proteins), whereas miR-146a inhibitor exerted opposite effects. Moreover, Dex modulated the levels of both miR-146a and its downstream target immunoglobulin superfamily Member 11 (IGSF11). The protective effects of miR-146a on COPD were reversed following IGSF11 intervention. Further, the phosphorylation of NF-κB and IKKγ suggested that the effects of Dex/miR-146a/IGSF11 axis on COPD were related to the NF-κB pathway.
Conclusion:
Our in vitro and in vivo studies showed that Dex alleviated CSE-induced COPD via modulating the miR-146a/IGSF11/NF-κB axis.
