Sulfur dioxide attenuates LPS-induced acute lung injury via enhancing polymorphonuclear neutrophil apoptosis  

作　　者：Hui-jie MA Xin-li HUANG Yan LIU Ya-min FAN 

机构地区：[1]Department of Physiology,Hebei Medical University,Shijiazhuang 050017,China [2]Department of Pathophysiology,Hebei MedicalUniversity,Shijiazhuang 050017,China [3]Department of Endocrinology,the Third Hospital of Hebei Medical University,Shijiazhuang050051,China

出　　处：《Acta Pharmacologica Sinica》2012年第8期983-990,共8页中国药理学报（英文版）

基　　金：This research program was supported by the National Natu-ral Science Foundation of China （No 81070050 and 30800440） and the Natural Science Foundation of Hebei Province （No C2007000830, C2008001040, and H2012206009）.

摘　　要：Aim： We speculated that the enhanced apoptosis of polymorphonuclear neutrophil （PMN） might be responsible for the inhibition of PMN infiltration in the lung. This study was designed to investigate the effects of sulfur dioxide （S02） on PMN apoptosis in vivo and in vitro, which may mediate the protective action of S02 on pulmonary diseases. Methods： Acute lung injury （ALl） was induced by intratracheally instillation of lipopolysaccharide （LPS, 100 IJg/lO0 g, in 200 pL saline） in adult male SD rats. S02 solution （25 pmol/kg） was administered intraperitoneally 30 rain before LPS treatment. The rats were killed 6 h after LPS treatment. Lung tissues were collected for histopathologic study and S02 concentration assay. Bronchoalveolar lavage fluid （BALF） was collected for the measurement of PMN apoptosis. For in vitro experiments, rat peripheral blood PMNs were cultured and treated with LPS （30 mg/L） and S02 （10, 20 and 30 pmol/L） for 6 h, and apoptosis-related protein expression was detected by Western blotting, and apoptosis rate was measured with flow cytometry. Results： LPS treatment significantly reduced the S02 concentrations in the lung tissue and peripheral blood, as compared with the control group. Pretreatment with S02 prevented LPS-induced reduction of the S02 concentration in the lung tissue and peripheral blood. LPS treatment significantly reduced PMN apoptosis both in vivo and in vitro, which could be prevented by the pretreatment with S02. The protein levels of caspase-3 and Bax was significantly increased, but Bcl-2 was decreased by the pretreatment with S02, as compared with LPS administration alone. Conclusion： S02 plays an important role as the modulator of PMN apoptosis during LPS-induced ALl, which might be one of the mechanisms underlying the protective action of S02 on pulmonary diseases.Aim： We speculated that the enhanced apoptosis of polymorphonuclear neutrophil （PMN） might be responsible for the inhibition of PMN infiltration in the lung. This study was designed to investigate the effects of sulfur dioxide （S02） on PMN apoptosis in vivo and in vitro, which may mediate the protective action of S02 on pulmonary diseases. Methods： Acute lung injury （ALl） was induced by intratracheally instillation of lipopolysaccharide （LPS, 100 IJg/lO0 g, in 200 pL saline） in adult male SD rats. S02 solution （25 pmol/kg） was administered intraperitoneally 30 rain before LPS treatment. The rats were killed 6 h after LPS treatment. Lung tissues were collected for histopathologic study and S02 concentration assay. Bronchoalveolar lavage fluid （BALF） was collected for the measurement of PMN apoptosis. For in vitro experiments, rat peripheral blood PMNs were cultured and treated with LPS （30 mg/L） and S02 （10, 20 and 30 pmol/L） for 6 h, and apoptosis-related protein expression was detected by Western blotting, and apoptosis rate was measured with flow cytometry. Results： LPS treatment significantly reduced the S02 concentrations in the lung tissue and peripheral blood, as compared with the control group. Pretreatment with S02 prevented LPS-induced reduction of the S02 concentration in the lung tissue and peripheral blood. LPS treatment significantly reduced PMN apoptosis both in vivo and in vitro, which could be prevented by the pretreatment with S02. The protein levels of caspase-3 and Bax was significantly increased, but Bcl-2 was decreased by the pretreatment with S02, as compared with LPS administration alone. Conclusion： S02 plays an important role as the modulator of PMN apoptosis during LPS-induced ALl, which might be one of the mechanisms underlying the protective action of S02 on pulmonary diseases.

关 键 词：acute lung injury bronchoalveolar lavage fluid （BALF） LIPOPOLYSACCHARIDE SO2 apoptosis polymorphonuclear granulocyte 

分 类 号：Q26[生物学—细胞生物学] TQ226.36[化学工程—有机化工]