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Eucalyptol protects lungs against bacterial invasion through attenuating ciliated cell damage and suppressing MUC5AC expression
Author(s) -
Yu Na,
Sun YiTian,
Su XinMing,
He Miao,
Dai Bing,
Kang Jian
Publication year - 2019
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.26359
Subject(s) - eucalyptol , lung , airway , bronchoalveolar lavage , respiratory epithelium , respiratory system , mucus , pathology , immunology , microbiology and biotechnology , biology , medicine , anatomy , anesthesia , food science , ecology , essential oil
This study was conducted to investigate whether eucalyptol plays a role in influencing bacterial growth in cigarette smoke‐exposed lungs. Rats were exposed to air (control) and cigarette smoke (smoking) in the presence and absence of eucalyptol (260 mg/day). Morphological analysis of lung structures and status of airway mucous production were observed under microscope. Pathological changes of ciliated columnar epithelium in airways were examined using transmission electron microscopy. MUC5AC protein and messenger RNA (mRNA) expression in bronchoalveolar lavage fluid (BALF) and lungs were determined. Application of eucalyptol reduced pulmonary bullae formation and airway mucus overproduction in the smoke‐exposed lungs. Treatment with eucalyptol attenuated ciliated cell damage in cigarette smoke‐exposed lungs. Bacterial colonies of lungs were obviously lower in the eucalyptol‐treated rats than that in the smoking rats ( p  < 0.01). Treatment with eucalyptol reduced the counts of bacterial colonization residing in the challenged lungs ( p  < 0.01). Application of eucalyptol not only decreased MUC5AC protein expression in BALF and tobacco‐exposed lungs but also suppressed its mRNA expression in the lungs (all p  < 0.05). Intervention of eucalyptol benefits elimination of bacterial organisms from tobacco‐exposed lungs through attenuating ciliated cell damage and suppressing MUC5AC expression in the lungs.

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