@Article{biocell.2021.014279,
AUTHOR = {CHEN-LIANG TSAI, YU-HUEI LIN, CHIH-YING CHANGCHIEN, CHIH-FENG CHIAN, CHI-HUEI CHIANG},
TITLE = {Benefit of prophylactic bronchodilator with β2 adrenergic agonist in ischemia-reperfusion-induced lung injury},
JOURNAL = {BIOCELL},
VOLUME = {45},
YEAR = {2021},
NUMBER = {5},
PAGES = {1201--1211},
URL = {http://www.techscience.com/biocell/v45n5/43077},
ISSN = {1667-5746},
ABSTRACT = {Primary lung graft dysfunction could significantly attribute to ischemia-reperfusion lung injury (IRLI) during
transplantation surgery. β2-adrenergic agonists were one of the bronchodilators that had been well-established in the
management of asthma and chronic obstructive pulmonary disease (COPD) with anti-inflammatory potency. By
applying the model of isolated rat lung, we evaluated the efficacy of short-acting β2-agonist inhalation to ameliorate
ischemia-reperfusion damage. The experiment protocol was 180 min of global ischemia and then reperfusion for
60 min. In the β2-agonist inhalation group, aerosolized albuterol was administrated prior ischemia procedure.
Increased weight ratios of wet to dry lung and microvascular permeability were characterized in the IRLI group. In
contrast, pre-inhaled β2-agonist significantly mitigated the severity of pulmonary edema. Bronchoalveolar lavage from
the β2-agonist group presented decreased leukocyte counts and cytokines production, including interleukin-1β
(IL-1β), tumor necrosis factor-α (TNF-α), and macrophage inflammatory protein 2 (MIP-2). Devastating oxidative
stress was widely recognized during the ischemia-reperfusion process, while β2-agonist pretreatment revealed subsided
H2O2, myeloperoxidase (MPO), and the cleavage of caspase-3. Western blotting from lung homogenates identified the
blockade of NF-κB and MAPK activation in the β2-agonist inhalation group. Currently, there was no specific
pharmacotherapy in IRLI management. Our results elucidated the protective effect of β2-agonist bronchodilator
against ischemia-reperfusion induced oxidative stress, inflammation reaction, and pulmonary edema.},
DOI = {10.32604/biocell.2021.014279}
}