Abstract: Poster Presentations |


Yang Deok Lee, MD*; Ju Young Kim, MS; Yoon Jin Kwak, MS; Ki Ho Lee, PhD; Tai Kyoung Baik, MD; Seong Kyu Lee, MD; Haing Woon Baik, MD; Dong Jib Na, MD; Min Soo Han, MD
Author and Funding Information

Eulji University Hospital, Daejeon, South Korea


Chest. 2008;134(4_MeetingAbstracts):p151002. doi:10.1378/chest.134.4_MeetingAbstracts.p151002
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PURPOSE: Sleep loss is associated with a small but significant decrease in pulmonary function in patients with COPD. In the patients with pulmonary diseases, sleep deprivation aggravates lung inflammation and vice versa. Recent researches have shown the relationship between sleep deprivation and inflammation. However, the underlying mechanisms of that phenomenon remain unclear. In the present study, we designed to investigate whether melatonin protects acute lung inflammation with sleep deprivation.

METHODS: Male ICR mice were deprived sleep using modified multiplatform water bath for 3 days. Acute lung inflammation was induced by lipopolysaccharide (LPS). Melatonin and LPS was administered in sleep-deprived (SD) mice at day 2. Mice were divided into 5 groups; control, SD only, LPS only, LPS+SD, and LPS+SD+melatonin (each group, n = 11). Animals were sacrificed at day 3, and lung tissues were collected for histological examination and analysis of apoptotic proteins. The level of malondialdehyde (MDA) was determined for the effect of oxidative stress.

RESULTS: Melatonin restored weight loss by LPS-induced acute lung inflammation in the SD. Histological findings revealed alveolar damages including inflammatory cell infiltration, hyaline membrane degeneration, and dilated alveolus in the LPS+SD. Melatonin remarkably attenuated alveolar damages. In western blot analysis, LPS reduced the levels of Bcl-XL and procaspase-3 in SD. By treatment of melatonin, the levels of Bcl-XL and procaspase-3 were increased, compared to the LPS+SD, respectively. LPS showed an increase of TUNEL-positive profiles in the lung tissue, whereas melatonin prevented the increase of cell death induced by LPS in the SD mice. In lipid peroxidation assay, melatonin significantly reduced the elevated MDA level in the LPS+SD from 7.0 ± 0.3 uM/g (mean ± S.E.) to 5.6 ± 0.2 (P < 0.05).

CONCLUSION: Sleep loss aggravates acute lung inflammation and melatonin has a protective effect against inflammation in sleep deprivation.

CLINICAL IMPLICATIONS: Melatonin treatment shows a recuperative effect of lung damage. Therefore, melatonin could be a therapeutic potential for clinical application of lung inflammation in sleep deprivation.

DISCLOSURE: Yang Deok Lee, No Financial Disclosure Information; No Product/Research Disclosure Information

Wednesday, October 29, 2008

1:00 PM - 2:15 PM




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