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Updated: Jun 7, 2025

Cigarette Smoke Exposure in Mice using a Whole-Body Inhalation System
Published on: October 22, 2020
Protection against cigarette smoke-induced chronic obstructive pulmonary disease via activation of the SIRT1/FoxO1
Qin Shen1, Jing Chen1, Suzhen Yang1
1Department of Respiratory Medicine, Hunan Provincial People's Hospital (The First Affiliated Hospital of Hunan Normal University) Changsha 410005, Hunan, P. R. China.
Objective:
To investigate the biological role of miR-132 in a murine model of chronic obstructive pulmonary disease (COPD) via activation of the SIRT1/FoxO1 axis.
Methods:
COPD was induced in C57BL/6J male mice by exposing them to cigarette smoke (CS) for 8 weeks. A miR-132 knockout mouse model was used to assess the role of miR-132 in CS-induced COPD. Lung tissue apoptosis was evaluated using TUNEL assays and histopathology, along with lung functional tests which were performed to assess CS-induced lung injury.
Results:
Elevated miR-132 expression was observed in lung tissues and bronchoalveolar lavage fluid in COPD mice. miR-132 depletion improved lung function, restored lung tissue morphology, and reduced apoptosis. Target prediction software identified miR-132 as a potential repressor of SIRT1. In COPD mice, SIRT1 and FoxO1 expression were reduced, but miR-132 knockout restored their levels.
Conclusion:
Inhibition of miR-132 may serve as a therapeutic strategy for CS-induced COPD.
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