Role of c-Jun N-terminal kinase in lipopolysaccharide-induced acute lung injury in rats
10.3760/cma.j.issn.0254-1416.2011.02.031
- VernacularTitle:c-Jun氨基末端激酶在大鼠内毒素性急性肺损伤中的作用
- Author:
Long CHEN
;
Qin CHENG
;
Xiyan CHEN
;
Yan ZHANG
;
Maoyin ZHANG
;
Wenwen ZHANG
;
Gongjian LIU
;
Mingzhang ZUO
- Publication Type:Journal Article
- Keywords:
JNK mitogen-activated protein kinases;
Endotoxemia;
Respiratory distress syndrome,adult
- From:
Chinese Journal of Anesthesiology
2011;31(2):237-239
- CountryChina
- Language:Chinese
-
Abstract:
Objective To evaluate the role of c-Jun N-terminal kinase (JNK) in lipopolysaccharide (LPS)-induced acute lung injury ( ALI) in rats.Methods Eighty male SD rats weighing 250-300 g were randomly divided into 4 groups ( n = 20 each) : control group (group C) ; ALI group; LPS + SP600125 (JNK inhibitor)group (group S) and LPS+ DMSO (the solvent) group (group DMSO) . ALI was induced by intravenous LPS 5mg/kg. In S and DMSO groups, SP600125 30 mg/kg and DMSO 0.2 ml were injected intravenously after LPS administration respectively. Ten animals were sacrificed by exsanguinafions at 4 h after LPS administration in each group. The broncho-alveolar lavage fluid (BALF) was colleted. The TNF-α and IL-1β concentrations in BALF were measured. The lungs were removed for microscopic examination and determination of W/D lung weight ratio. The other 10 animals in each group were observed for 48 h survival rate. Results Intravenous LPS significantly increased TNF-α and IL-1β concentrations in BALF and W/D lung weight ratio, decreased 48 h survival rate and induced histologic damage. Intravenous SP600125 30 mg/kg significantly attenuated the above-mentioned LPS-induced changes. Conclusion Activation of JNK is involved in the development of endotoxin-induced ALI in rats.
