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应用反义技术探讨ｃｆｏｓ基因在ＥＴ１调控肺泡Ⅱ型细胞（ＡＴⅡ）表面活性物质（ＰＳ）合成的胞内信号转导中的作用。结果显示：（１）内皮素１（ＥＴ１）可提高ＡＴⅡ细胞的３Ｈ胆碱掺入量。（２）蛋白激酶Ｃ（ＰＫＣ）激活剂ＰＭＡ可使ＡＴⅡ细胞的３Ｈ胆碱掺入量增加，ＰＫＣ抑制剂Ｈ７可抑制ＥＴ１的促ＰＳ合成效应。（３）ＥＴ１和ＰＭＡ可显著提高Ｆｏｓ蛋白表达量。Ｈ７和ｃｆｏｓ反义寡核苷酸（ＯＤＮ）预处理可抑制ＥＴ１促Ｆｏｓ蛋白表达和促３Ｈ胆碱掺入效应。（４）ＥＴ１、正义及反义ＯＤＮ对ＡＴⅡ细胞乳酸脱氢酶（ＬＤＨ）释放量均无显著影响。结果证实：ＥＴ１可促进ＡＴⅡ的ＰＳ合成，激活ＰＫＣ上调ｃｆｏｓ基因表达是ＥＴ１促ＡＴⅡ细胞合成ＰＳ的胞内信号转导途径。
The antisense technique was used to investigate the role of c-fos gene in the intracellular signal transduction of ET-1 in the regulation of surfactant (PSII) synthesis in alveolar type II cells (ATII). The results showed that: (1) Endothelin 1 (ET 1) can increase 3H Ⅱ choline incorporation of AT Ⅱ cells. (2) PMA, a protein kinase C (PKC) activator, increased 3H-choline incorporation in ATⅡ cells, and PKC inhibitor H7 inhibited ET-1-induced PS synthesis. (3) ET 1 and PMA can significantly increase the expression of Fos protein. H7 and c fos antisense oligonucleotide (ODN) pretreatment can inhibit ET 1 promote Fos protein expression and promote 3H choline incorporation. (4) ET-1, sense and antisense ODN had no significant effect on the release of lactate dehydrogenase (LDH) in ATⅡ cells. The results confirmed: ET 1 can promote AT Ⅱ PS synthesis, activation of PKC up c fos gene expression is ET 1 promote AT Ⅱ cells to synthesize PS intracellular signal transduction pathway.