Effect of aminoguanidine on inflammatory reaction and nuclear Factor-?B signal pathway in the lipopolysaccharide-induced acute lung injury in rats
- VernacularTitle:氨基胍对内毒素性肺损伤炎症反应和NF-?B信号通路的影响
- Author:
Liping LI
;
Jianxin ZHANG
;
Lanfang LI
- Publication Type:Journal Article
- Keywords:
acute lung injury;
aminoguanidine;
LPS;
NF-?B;
ICAM-1;
inflammatory factors;
nitric oxide synthase
- From:
Chinese Pharmacological Bulletin
2003;0(11):-
- CountryChina
- Language:Chinese
-
Abstract:
Aim To investigate the effect and the possible mechanism of aminoguanidine(AG)on the lipopolysaccharide(LPS)-induced acute lung injury in rats.Methods Male SD rats were randomly divided into control group,LPS group and AG group.AG was administered in AG group,saline was administered in control group and LPS group.All the groups were further divided into 2 subgroups according to the duration of ALI:3 h+3 h group and 6 h+3 h group.In AG group and LPS group,LPS was administered.Saline was administered in control group.The translocation of NF-?B and the expression of intercellular adhesion molecule-1(ICAM-1)were respectively detected with immunohistochemisty(IHC);the concentrations of TNF-? and IL-6 in lung tissue were evaluated by radioimmunoassay;the pathological changes of lung tissue were observed by light and electron microscope.Results Compared with those of the control group,NF-?B was significantly translocated from the cytoplasm into the nucleus,the expression of NF-?B and ICAM-1 protein were significantly increased.The concentrations of TNF-? and IL-6 in lung tissue were significantly increased in LPS group.Degree of ALI was gradually worsened after administration of LPS.In AG(3 h+3 h)group,the expression of NF-?B and ICAM-1 protein were significantly decreased,the concentrations of TNF-? and IL-6 in lung tissue were significantly decreased and the lung damage was improved compared with those of the LPS(3 h+3 h)group.Conclusions Administration of AG could ameliorate LPS-induced acute lung injury in rats.The possible mechanism was that AG could reduce the expression of iNOS mRNA,inhibited NF-?B activation and subsequently led to the down-regulation of NF-?B-dependent inflammatory gene expression and thus reduced the inflammatory response in lung injury.
