Effect of exogenous hydrogen sulfide on polymorphonuclear neutrophil accumulation in acute lung injury rat induced by lipopolysaccharides and its mechanism / 中国应用生理学杂志
Chinese Journal of Applied Physiology
; (6): 477-480, 2010.
Artigo
em Chinês
| WPRIM (Pacífico Ocidental)
| ID: wpr-301531
Biblioteca responsável:
WPRO
ABSTRACT
<p><b>OBJECTIVE</b>To study the effects of sodium hydrosulfide (NaHS), hydrogen sulfide (H2S) donor, on LPS-induced polymorphonuclear neutrophil (PMN) accumulation and its mechanism.</p><p><b>METHODS</b>The animal model of acute lung injury (ALI) caused by intravenous injection of lipopolysaccharides (LPS). Adult male Spraguce-Dawley (SD) rats were randomly divided into four groups (n = 8 - 12 per group) Control group (0.5 ml/kg normal saline i.v.), LPS-treated group (1 mg/kg, i.v.), LPS plus NaHS (1 mg/kg i.v. and 28 micromol/kg i.p., respectively) and NaHS group (28 micromol/kg i.p.). Animals were sacrificed at 6 h after agent administration. Morphological changes of lung tissues were observed and polymorphonuclear neutrophil (PMN) number in alveolar septum was tested. The apoptosis of PMN in the bronchoalveolar lavage fluid (BALF) was examined with in situ TdT-mediated dUTP end labeling (TUNEL). Intercellular adhesion factor-1 (ICAM-1) and nuclear factor-kappaB (NF-kappaB) expressions in the lung tissue were analyzed by Western Blot.</p><p><b>RESULTS</b>The results showed that bleeding, edema, PMN accumulation and other pathological signs in the lung tissue emerged after LPS injection. Compared to control rats, the LPS-treated rats had increased PMN number, decreased PMN apoptotic percentages, and increased expressions of ICAM-1 and NF-kappaB. Administration of NaHS into LPS-treated rats reduced the PMN number and expressions of ICAM-1 and NF-kappaB but increased PMN apoptotic percentages. In addition, NaHS alleviated the degree of ALI. There were no significant differences of the above indicators between NaHS-treated rats and control rats.</p><p><b>CONCLUSION</b>NaHS can reduce the PMN accumulation in the lung, and its mechanism is related to down-regulation expression of ICAM-1 and promotion of PMN apoptosis induced by inhibition of NF-kappaB pathway.</p>
Texto completo:
Disponível
Contexto em Saúde:
ODS3 - Meta 3.4 Reduzir as mortes prematuras devido doenças não transmissíveis
Problema de saúde:
Outras Doenças Sanguíneas
/
Outras Doenças Respiratórias
Base de dados:
WPRIM (Pacífico Ocidental)
Assunto principal:
Patologia
/
Farmacologia
/
Lipopolissacarídeos
/
NF-kappa B
/
Ratos Sprague-Dawley
/
Apoptose
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Molécula 1 de Adesão Intercelular
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Biologia Celular
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Lesão Pulmonar Aguda
/
Sulfeto de Hidrogênio
Tipo de estudo:
Estudo prognóstico
Limite:
Animais
Idioma:
Chinês
Revista:
Chinese Journal of Applied Physiology
Ano de publicação:
2010
Tipo de documento:
Artigo