... metalloproteinases，TIMPs)之间的不平衡．过度的凝胶分解活性 (nclatinolytic activity)和肺泡上皮凋亡(epithelial apoptosis)9'七同参与 了肺纤维化的产生。但是这些研究仍处于起始阶段，更进一步的研究将能够揭示 这些机制的深层次的关系。
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RAS抑制可以通过多种分子机制抑制肺泡上皮细胞和血管内皮细胞的凋亡，抑制炎症级联反应和细胞外基质沉积，而使肺纤维化病变减轻。
RAS inhibition can reduce cell apoptosis of alveolar epithelial cells and endothelial cells, interfere with the inflammation cascade, and decrease fibroblast activity during tissue repair process.
结论：在肺纤维化形成过程中，内源性NO的增多，有诱导肺泡上皮细胞凋亡的作用。
CONCLUSION: the apoptosis of alveolar epithelial cell is induced by high level of endogenous no in the development of pulmonary fibrosis.
目的：研究大鼠肺纤维化形成过程中异常增多的肺内源性一氧化氮对肺泡上皮细胞凋亡的影响。
AIM: to study the role of high level of endogenous nitric oxide (no) in apoptosis of alveolar epithelial cells in the development of pulmonary fibrosis in rats.
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