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目的：探讨急性低氧油酸肺损伤大鼠肺组织中ＳＰ－Ａ和ＳＰ－Ｂ的表达，明确ＳＰ－Ａ和ＳＰ－Ｂ在肺表面活性物质（ＰＳ）中的作用，及其对该系统的影响。方法：采用低氧大鼠油酸肺损伤模型及免疫组化技术，采用己酮可可碱对急性肺损伤进行干预。结果：ＳＰ－Ａ和ＳＰ－Ｂ在肺内的表达主要以肺泡Ⅱ型上皮细胞为对象，ＳＰ－Ｂ的特异性较ＳＰ－Ａ高。肺泡腔和小支气管腔内可见一层免疫阳性物质沉着，肺泡Ⅱ型上皮细胞多位于肺泡隔部和角部并靠近肺泡腔。己酮可可碱可使ＳＰ－Ａ蛋白表达增加。结论：ＳＰ－Ａ和ＳＰ－Ｂ在肺内的表达主要以肺泡Ⅱ型上皮细胞为对象，气道上皮和血管内皮以及间质细胞均未见明显的表达，ＳＰ－Ｂ的特异性较ＳＰ－Ａ高。急性低氧油酸肺损伤时，肺组织ＳＰ－Ａ和ＳＰ－Ｂ免疫组化显示肺泡Ⅱ型上皮细胞的表达明显减弱。己酮可可碱可使ＳＰ－Ａ蛋白表达增加。
OBJECTIVE: To investigate the expression of SP-A and SP-B in the lung tissue of acute hypoxia-induced oleic acid-induced lung injury in rats and the role of SP-A and SP-B in pulmonary surfactant (PS) Impact. Methods: Hypoxic rat model of oleic acid-induced lung injury and immunohistochemistry were used. Pentoxifylline was used to interfere acute lung injury. Results: The expression of SP-A and SP-B in the lung was mainly in type II alveolar epithelial cells. SP-B was more specific than SP-A. Alveolar cavity and small bronchial cavity can be seen in a layer of immunopositive substances calm, alveolar type Ⅱ epithelial cells located in the alveolar septum and corner and near the alveolar space. Pentoxifylline increased SP-A protein expression. CONCLUSIONS: The expression of SP-A and SP-B in the lung mainly targets type II alveolar epithelial cells with no obvious expression in airway epithelium, endothelium and interstitial cells. SP-B is more specific than SP- A high. Acute hypoxia-induced oleic acid-induced lung injury, lung tissue SP-A and SP-B immunohistochemistry showed that the expression of type II alveolar epithelial cells was significantly weakened. Pentoxifylline increased SP-A protein expression.