LPS致大鼠肺泡Ⅱ型细胞凋亡及对Fas抗原表达的影响

EFFECTS OF LPS ON APOPTOSIS AND FAS EXPRESSION IN PULMONARY ALVEOLAR TYPE Ⅱ CELLS

探讨Ｆａｓ信号通路在肺泡Ⅱ型细胞损伤作用的可能机制及意义．建立大鼠肺泡Ⅱ型细胞体外培养，采用流式细胞术、原位杂交、逆转录、多聚酶链式反应等方法，观察大肠杆菌内毒素（ＬＰＳ）对肺泡Ⅱ型细胞ＦａｓｍＲＮＡ、蛋白质及细胞凋亡的影响．成功建立大鼠肺泡Ⅱ型细胞体外培养技术，ＬＰＳ刺激后，肺泡Ⅱ型细胞ＦａｓｍＲＮＡ、蛋白质表达均显著增加（Ｐ＜０．０１），ＬＰＳ可诱导肺泡Ⅱ型细胞凋亡，并在一定范围内呈量－效关系，表明ＬＰＳ对肺泡上皮的损伤效应，除直接损伤作用外，还可能通过诱导Ｆａｓ抗原表达增加。

To explore the mechanism of Fas signal pathway on damage of alueolar type Ⅱ cells. By using cytometry techniques, ISH、 RT PCR, Fas mRNA、 protein and apoptosis were studied in alveolar type Ⅱ cells. We successfully developed a method for isolation and culture of alveolar type Ⅱ cells in rate. Fas mRNA and protein expression were in creased markedly ( P <0.01) after treated with LPS. Induction of apoptosis in rat alveolar type Ⅱ cell after administration of LPS; which was dependent on the dose of LPS. We speculate apoptosis and Fas signal pathway may play a role in LPS induced damage of alveolar type Ⅱ cells.