Role of polymorphonuclear neutrophil in exogenous hydrogen sulfide attenuating endotoxin-induced acute lung injury.
- Author:
Xin-Li HUANG
1
;
Xiao-Hong ZHOU
;
Jun-Lin ZHOU
;
Chun-Hua DING
;
Xiao-Hui XIAN
Author Information
1. Department of Pathophysiology, Hebei Medical University, Shijiazhuang 050017, China. huangxinli2006@hotmail.com
- Publication Type:Journal Article
- MeSH:
Acute Lung Injury;
chemically induced;
immunology;
pathology;
Animals;
Apoptosis;
Disease Models, Animal;
Humans;
Hydrogen Sulfide;
pharmacology;
Lipopolysaccharides;
adverse effects;
Lung;
pathology;
Neutrophils;
immunology;
Rats;
Sulfides;
pharmacology
- From:
Acta Physiologica Sinica
2009;61(4):356-360
- CountryChina
- Language:Chinese
-
Abstract:
The animal model of acute lung injury (ALI) caused by intravenous injection of lipopolysaccharides (LPS) and cultured human peripheral blood polymorphonuclear neutrophil (PMN) were used to study the effects of sodium hydrosulfide (NaHS), hydrogen sulfide (H2S) donor, on LPS-induced PMN accumulation, microvascular permeability and PMN apoptosis. Control group, NaHS group, LPS group and LPS + NaHS group were established both in in vivo and in vitro studies. Microvascular permeability, PMN accumulation in lung and apoptosis of PMN were detected. The results showed that: (1) In in vivo study, PMN accumulation in lung, the protein content in bronchoalveolar lavage fluid (BALF) and the Evans blue dye in lung tissue of LPS group were markedly higher than those of both sham operation group and LPS + NaHS group (P<0.05, P<0.01); (2) In in vitro study, the apoptotic rates of PMN in LPS group and NaHS group were significantly higher than that in control group (P<0.01), while compared with LPS group, LPS + NaHS group showed significantly higher apoptotic rate (P<0.01). These results suggest that NaHS attenuates LPS-induced microvascular permeability and alleviates ALI. PMN apoptosis induced by NaHS is possibly one of the potential mechanisms underlying the decrease of PMN accumulation in lung tissue.
