摘要
目的通过观察脂多糖(LPS)刺激对肺微血管内皮细胞水通道蛋白-1mRNA表达和功能的影响,以探讨急性肺损伤肺水异常代谢的机制。方法在体外培养的大鼠肺微血管内皮细胞(RLMEC),分别使用浓度为100μg/L、1mg/L、10mg/L的LPS与之孵育4h、12h、24h后,应用氚水掺入法测定RLMEC内氚水的信号强度,并用RT-PCR法测定AQP-1mRNA的表达。结果LPS刺激组氚水的信号强度显著低于对照组(P<001);同时LPS刺激组AQP-1mRNA的表达显著低于对照组。结论LPS刺激RLMECAQP-1mRNA表达和摄水功能下降,提示AQP-1在急性肺损伤时可能与肺水代谢异常有关。
AIM: To determine if aquaporin-1 (AQP-1) expression and function is influenced after lipopolysaccharide (LPS) stimulation in rat lung microvessel endothelial cells and to investigate the mechanisms of lung fluid abnormal metabolism in acute lung injury. METHODS: LPS at different concentrations (100 μg/L, 1 mg/L or 10 mg/L) was used to stimulate cultivated rat lung microvessel endothelial cells in vitro at different stimulatory times (4 h, 12 h or 24 h), respectively. Tritium water permeation was conducted for determining the intracellular signal intensity in rat lung microvessel endothelial cells. The RT-PCR technique was applied for the assay of the expression of AQP-1 mRNA. RESULTS: The signal intensity of intracellular tritium water in the LPS stimulation group was less than that in normal control significantly. Compared with the normal control group (P<0.01), there was obvious decrease in the expression of AQP-1 mRNA in LPS stimulation groups. CONCLUSION: The decreased expression of AQP-1 mRNA and the weaken function of transporting water suggest that AQP-1 may play a major role in abnormal fluid transportation in acute injured lung. [
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2005年第1期104-107,共4页
Chinese Journal of Pathophysiology
基金
军队"十五"医药卫生科研基金重点课题
关键词
脂多糖类
水孔蛋白类
肺
血管内皮细胞
急性肺损伤
Lipopolysaccharides
Aquaporins
Lung
Vascular endothelial cells
Acute lung injury
