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目的 通过观察大鼠常压缺氧肺动脉高压模型肺组织信号传导与转录活化因子(STATs)的表达水平 ,探讨其在低氧性肺动脉高压 (HPH)形成过程中参与的可能机制。方法 健康成年雄性Wistar大鼠 6 0只 ,随机分为缺氧组和健康对照组 ,缺氧组大鼠复制HPH模型。用逆转录 (RT) 聚合酶链反应 (PCR)和Northernblot检测 2组大鼠肺组织STATsmRNA的表达水平 ,免疫组化检测大鼠肺组织STATs蛋白的含量。结果 RT PCR扩增显示 ,缺氧 1周大鼠肺组织STAT 1、STAT 2、STAT 3、STAT5mRNA表达水平升高 ,缺氧 2周表达水平最高 ,缺氧 3周表达水平降低 ,但明显高于健康对照组 ;且缺氧 2周的表达水平高于其他缺氧时间 (P <0 0 5 ) ;STAT 4未检出。Northernblot显示 ,缺氧 2周大鼠肺组织STAT 1、STAT 3、STAT 5mRNA表达高于其他缺氧时间 (P <0 0 1)。缺氧 3周大鼠肺组织STAT3和STAT 5组化染色可见 ,肺泡壁细胞、支气管壁细胞、小血管壁细胞及巨噬细胞的胞核呈紫蓝色 ;图像定量分析显示 ,缺氧 3周大鼠肺组织STAT 3和STAT 5蛋白表达含量最高 ,缺氧 4周含量降低 ,但仍高于健康对照组 (P <0 0 1)。结论 大鼠常压缺氧肺动脉高压模型肺组织STATsmRNA和蛋白表达增高 ,提示STAT可能参与了HPH的发病机制。
OBJECTIVE: To investigate the expression of signal transducers and activators of transcription (STATs) in the lung tissue of hypoxic pulmonary hypertensive rats under hypobaric hypobaric hypobaric hypoxia (Hypoxic pulmonary hypertension) and to explore the possible mechanism involved in the pathogenesis of hypoxic pulmonary hypertension (HPH). Methods Sixty adult male Wistar rats were randomly divided into hypoxia group and healthy control group. Rats in hypoxia group were given HPH model. The expression of STATsmRNA in the lungs of the two groups was detected by reverse transcription (RT) polymerase chain reaction (PCR) and Northern blotting. The expression of STATs protein in the lung tissue was detected by immunohistochemistry. Results RT-PCR showed that the expression of STAT1, STAT2, STAT3 and STAT5 mRNA in the lungs of hypoxia rats increased one week after hypoxia, the highest expression was found at 2 weeks of hypoxia and decreased at 3 weeks of hypoxia, but significantly higher than that of hypoxia Healthy control group. The expression level in hypoxia for 2 weeks was higher than that in other hypoxia time (P <0.05); STAT 4 was not detected. Northern blot showed that the expression of STAT 1, STAT 3 and STAT 5 mRNA in the lungs of hypoxia rats for 2 weeks were higher than those of other hypoxia groups (P <0.01). After 3 weeks of hypoxia, STAT3 and STAT5 staining showed that the nuclei of alveolar wall cells, bronchial wall cells, small blood vessel wall cells and macrophages were purple-blue. Image quantitative analysis showed that hypoxia for 3 weeks The content of STAT 3 and STAT 5 protein in the lungs of rats was the highest, but decreased in the 4th week of hypoxia, but still higher than that of the healthy control group (P <0.01). Conclusion The STATmRNA and protein expression in the lung tissue of rats with hypoxia-induced pulmonary hypertension were increased, indicating STAT may be involved in the pathogenesis of HPH.