摘要
目的探讨肺组织细胞间黏附分子-1(ICAM-1)表达与急性肺损伤(ALI)的关系以及中药生脉饮对其影响。方法注射脂多糖(LPS)复制大鼠ALI模型,根据干预因素不同随机分为四组,即生理盐水对照组、LPS组、生脉饮+LPS组、地塞米松+LPS组。观察肺组织病理形态和ALI生物学标志并测定肺组织ICAM—1mRNA。结果肺血管内皮细胞ICAM-1mRNA表达在LPS组显著高于对照组(P〈0.01),生脉饮+LPS组和地塞米松+LPS组显著弱于LPS组(P〈0.05,P〈0.01);肺渺干质量比,肺泡灌洗液中性粒细胞比、蛋白含量以及肺血管壁通透性、肺泡通透指数也显著小于LPS组。结论肺组织ICAM-1mRNA表达增强参与了Au发生、发展,生脉饮和地塞米松可使肺组织损伤减轻,其机制可能是抑制了肺组织ICAM-1mRNA表达。
Objective To approach the relationship between the expression of intercellular adhesion molecule ( ICAM - 1 mRNA) and acute lung injury (ALI ) as well as the mechanisms of shengmaiyin in the prevention and treatment of ALI. Methods ALI animal models were performed by injecting Lipopolysaccharide (LPS) through the sublingually vien of rats. The rats were divided randomly into 4 groups: control group, LPS group, shengmaiyin + LPS group and dexamethasone + LPS group. Histopathological examinations and biological markers were measured. Molecular hybridization method was used to determine the expression of ICAM - 1 mRNA. Result The ICAM - 1 mRNA expression in the lung tissues of LPS group significantly increased comparing with control group ( P 〈 0.01 ). Furthermore, it was lower in shengmaiyin and dexamethasone group than that in LPS group ( P 〈 0.05 ,P 〈 0.01, respectively). Meanwhile, pathologic changes and the biological markers of ALI significantly decreased or ameliorated. Conclusions The expression of ICAM - 1 mRNA was involved in the formation of ALI. shengmaiyin and dexamethasone can ameliorate the lung damage during ALI, the mechanism may be related to inhibiting the expression of ICAM - 1 mRNA.
出处
《中国急救医学》
CAS
CSCD
北大核心
2009年第4期327-329,386,共4页
Chinese Journal of Critical Care Medicine
关键词
脂多糖
细胞黏附分子
急性肺损伤
生脉饮
地塞米松
Lipopolysaccharides ( LPS )
Intercellular adhesion molecule - 1 ( ICAM - 1 )
Acute lung injury (ALI)
Shengmaiyin
Dexamethasone