Influence of methylprednisolone on mouse alveolar type 2 cell response to acute lung injury.
Influence of methylprednisolone on mouse alveolar type 2 cell response to acute lung injury.
复制标题
甲基强的松龙对小鼠肺泡 2 型细胞对急性肺损伤反应的影响。
DOI：
10.1164/arrd.1981.123.4.459
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发表时间：
1981
期刊：
影响因子：
--
通讯作者：
Brody,JS
中科院分区：
文献类型：
--
作者：
Smith,LJ;Brody,JS
为了确定皮质类固醇是否影响急性肺损伤后肺泡2型细胞事件，我们在单次注射丁基羟基甲苯（BHT）后的不同时间给予小鼠30 mg/kg/天的甲基强的松龙（MP）。用氚标记胸苷（3 H-T）放射自显影研究2型细胞的增殖和分化。用3 H-T标记的板层体体积密度和面积的超微结构分析评价2型细胞的成熟。BHT损伤1型细胞并诱导2型细胞增殖。在第3天用3 H-T标记的2型细胞中有60%在4天内分化为1型细胞。每个细胞的板层体面积不变。MP早期给药（第1天和第2天）抑制2型细胞增殖时，肺损伤是轻度的;反弹增殖发生后，其中断。当肺损伤严重时，MP不能抑制增殖。延长MP给药（第1 - 5天）导致2型细胞增殖、肺损伤和死亡率增加。晚期MP给药（第3天和第4天）损害了2型细胞向1型细胞的分化，并且新的2型细胞的每个细胞的板层体面积增加了一倍以上。肺泡2型细胞的增殖、分化和成熟之间似乎存在重要的相互作用，这表明影响这些过程之一的药物可能影响2型细胞功能的所有方面。
To determine whether corticosteroids influence alveolar type 2 cell events after acute lung injury, we administered 30 mg/kg/day of methylprednisolone (MP) to mice at various times after a single injection of butylated hydroxytoluene (BHT). Tritiated thymidine (3H-T) autoradiographs were used to study type 2 cell proliferation and differentiation. Type 2 cell maturation was evaluated by ultrastructural analysis of lamellar body volume density and area in cells labeled with3H-T. The BHT damaged type 1 cells and induced proliferation of type 2 cells. Sixty per cent of type 2 cells labeled with3H-T on Day 3 differentiated into type 1 cells over a 4-day period. Lamellar body area per cell was unchanged. Early administration of MP (Days 1 and 2) inhibited type 2 cell proliferation when lung injury was mild; rebound proliferation occurred after its discontinuation. The MP failed to inhibit proliferation when lung injury was severe. Prolonged MP administration (Days 1 to 5) resulted in greater type 2 cell proliferation, lung injury, and mortality. Late MP administration (Days 3 and 4) impaired differentiation of type 2 to type 1 cells and more than doubled lamellar body area per cell of new type 2 cells. Important interactions appear to exist between proliferation, differentiation, and maturation of alveolar type 2 cells suggesting that agents that influence one of these processes may influence all aspects of type 2 cell function.