Bilirubin treatment suppresses pulmonary inflammation in a rat model of smoke-induced emphysema
Bilirubin treatment suppresses pulmonary inflammation in a rat model of smoke-induced emphysema
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DOI：
10.1016/j.bbrc.2015.07.133
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发表时间：
2015-09-18
影响因子：
3.1
通讯作者：
Li, Jianqiang
中科院分区：
文献类型：
--
作者：
Wei, Jingjing;Zhao, Hui;Li, Jianqiang
Background: Cigarette smoking is a significant risk factor for emphysema, which is characterized by airway inflammation and oxidative damage.Objectives: To assess the capacity of bilirubin to protect against smoke-induced emphysema. Methods: Smoking status and bilirubin levels were recorded in 58 patients with chronic obstructive pulmonary diseases (COPD) and 71 non-COPD participants. The impact of smoking on serum bilirubin levels and exogenous bilirubin (20 mg/kg/day) on pulmonary injury was assessed in a rat model of smoking-induced emphysema. At sacrifice lung histology, airway leukocyte accumulation and cytokine and chemokine levels in serum, bronchoalveolar lavage fluid (BALF) and lung were analyzed. Oxidative lipid damage and anti-oxidative components was assessed by measuring malondialdehyde, superoxide dismutase (SOD) activity and glutathione.Results: Total serum bilirubin levels were lower in smokers with or without COPD than non-smoking patients without COPD (P < 0.05). Indirect serum bilirubin levels were lower in COPD patients than patients without COPD (P < 0.05). In rats, cigarette smoke reduced serum total and indirect bilirubin levels. Administration of bilirubin reduced mean linear intercept and mean alveoli area, increased mean alveoli number, reduced macrophage, neutrophil and TNF-a content of BALF, and increased BALF and serum IL-10 level, but lowered local and systemic CCL2, CXCL2, OCCL8 and IL-17 levels. Bilirubin suppressed the smoke-induced systemic and regional oxidative lipid damage associated with increased SOD activity.Conclusion: Bilirubin attenuated smoking-induced pulmonary injury by suppressing inflammatory cell recruitment and pro-inflammatory cytokine secretion, increasing anti-inflammatory cytokine levels, and anti-oxidant SOD activity in a rat model of smoke-induced emphysema. (C) 2015 Published by Elsevier Inc.
