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Respiration 2011

Protective effect of nicotine on lipopolysaccharide-induced acute lung injury in mice.

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Yun Feng Ni
Feng Tian
Zi Fan Lu
Guo Dong Yang
Hai Yan Fu
Jian Wang
Xiao Long Yan
Ya Chao Zhao
Yun Jie Wang
Tao Jiang

키워드

요약

BACKGROUND

Recently, nicotine administration has been shown to be a potent inhibitor of a variety of innate immune responses, including endotoxin-induced sepsis.

OBJECTIVE

It was the aim of this study to evaluate the effect of nicotine on attenuating lung injury and improving the survival in mice with lipopolysaccharide (LPS)-induced acute lung injury (ALI).

METHODS

ALI was induced in mice by intratracheal instillation of LPS (3 mg/ml). The mice received intratracheal instillation of nicotine (50, 250 and 500 μg/kg) before or after LPS administration. Pulmonary histological changes were evaluated by hematoxylin-eosin stain, and lung wet/dry weight ratios were observed. Concentrations of tumor necrosis factor (TNF)-α, interleukin (IL)-1β and high mobility group box (HMGB)-1, as well as myeloperoxidase (MPO) activity were measured by enzyme-linked immunosorbent assay. The mortality rate was recorded and analyzed by the Kaplan-Meier method.

RESULTS

Nicotine pretreatment significantly attenuated the severity of lung injury and inhibited the production of TNF-α, IL-1β and HMGB-1 in mice with ALI. After LPS administration, the lung wet/dry weight ratios, as an index of lung edema, and MPO activity were also markedly reduced by nicotine pretreatment. Early treatment with a high dose of nicotine (500 μg/kg) after LPS administration decreased the mortality in mice with ALI, even when treatment was started 24 h after LPS administration.

CONCLUSIONS

Nicotine attenuated the lung injury and reduced mortality in mice with LPS-induced ALI.

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