摘要
采用放射免疫分析法观察大鼠肺泡巨噬细胞（ＡＭ）的内皮素（ＥＴ）生成。结果显示：①未受刺激的ＡＭ存在ＥＴ的基础分泌；②脂多糖（ＬＰＳ）、佛波醇酯（ＰＭＡ）和Ｃａ２＋导入剂Ａ２３１８７均可显著促进ＡＭ的ＥＴ生成；③钙调蛋白（ＣａＭ）抑制剂Ｗ７可阻断ＰＭＡ的促ＥＴ生成效应；④外源性前列腺素Ｅ２（ＰＧＥ２）可抑制ＬＰＳ和ＰＭＡ的促ＥＴ生成效应，消炎痛可增强ＬＰＳ的作用。结果表明，ＡＭ具有产生ＥＴ的功能，调控ＡＭ生成ＥＴ的细胞内信号转导途径存在依赖ＰＫＣ和Ｃａ２＋－ＣａＭ二条途径。
Using radioimmunoassay, we studied the endothelin(ET) production of alveolar macrophages(AM) of the rats. The results showed that: (1) a basal amount of ET which was timedependent (r=0.7415,P<0.01) was detected in supernatant of cultured unstimulated AM; (2) lipopolysaccharide (LPS), PMA, or A23187 could increase the ET production of AM (P<0.01); (3) calmodulin antagnoist W7 reduced the ET production of LPS or A23187stimulated AM (P<0.05,P<0.01), but did not effect that of PMAstimulated AM; protein kinase C inhibitor H7 attenuated the effect of PMA on ET production (P<0.01), but did not effect LPS on ET production; (4) prostaglandin E_2(PGE_2) inhibited the ET production of LPSstimulated (P<0.05) and PMAstimulated AM (P<0.05); cyclooxygenase inhibitor indomethacin enhanced the effect of LPS on ET production (P<0.01), but did not effect PMA on ET production. We conclude that AM is an important source of ET in the lungs both at physiologic and pathologic situation; there are two pathways of signal transduction for factors stimulating ET production of AM, i.e., PKCdependent and Ca^(2+)calmodulindependent pathways; the autocrine PGEs from AM shows a negatively modulated effect on ET production of AM.
出处
《湖南医科大学学报》
CSCD
1998年第3期221-224,共4页
Bulletin of Hunan Medical University
基金
国家自然科学基金
关键词
肺泡
巨噬细胞
内皮素
前列腺素E2
大鼠
pulmonary alveoli
macrophages
endothelin
prestaglandins E
protein kinase C
calmodulin
rats
