Alteration of pulmonary surfactant proteins in rats chronically exposed to cigarette smoke.
Alteration of pulmonary surfactant proteins in rats chronically exposed to cigarette smoke.
复制标题
长期暴露于香烟烟雾的大鼠肺表面活性蛋白的变化。
DOI：
10.1006/taap.1996.0222
复制
发表时间：
1996
期刊：
影响因子：
--
通讯作者：
Gairola,CG
中科院分区：
文献类型：
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作者：
Subramaniam,S;Whitsett,JA;Hull,W;Gairola,CG
肺表面活性物质（SurfactantProteins，SP）在增强肺表面活性物质的表面性质和参与肺的宿主防御机制中起重要作用。尽管已知吸烟会改变肺表面活性物质的脂质组成和功能，但其对SP的影响尚不清楚。本研究旨在确定慢性暴露于香烟烟雾是否会改变大鼠模型中的肺SP，即SP-A和SP-B。将Sprague-Dawley大鼠暴露于香烟烟雾中，每天两次，每天一次，持续70周。处死时，从房间对照、假处理（SH）和烟雾暴露（SM）动物中采集支气管肺泡灌洗液（BAL）和肺组织进行分析。SM大鼠的BAL液中的总蛋白水平有升高的趋势，但与SH组相比无统计学差异。然而，在SM大鼠的BAL液中的白蛋白含量，通过定量免疫印迹法测定，显着高于对照组。与对照组相比，SM大鼠BAL液中SP-A和SP-B水平分别显著降低25%和50%，以单位/微克BAL液蛋白表示。然而，当以每只大鼠回收的总BAL液SP计算时，只有SM大鼠的SP-B水平与对照组有显著差异。通过ELISA的进一步分析证实了SM大鼠中SP-B水平的降低。与BAL液相比，对照组和烟雾暴露组的肺组织SP水平及其各自的mRNA无显著差异。这些结果表明，选择性减少SP-B含量的支气管肺泡表面慢性暴露于香烟烟雾，并建议香烟烟雾对表面活性剂分泌过程和/或局部破坏SP的支气管肺泡表面的抑制作用。
Surfactant proteins (SP) play an important role in enhancing the surface properties of pulmonary surfactant and participate in host–defense mechanism(s) of the lung. Although it is known that cigarette smoking alters both pulmonary surfactant lipid composition and function, its effect on SPs is unknown. The present study was carried out to determine if chronic exposure to cigarette smoke alters pulmonary SPs, namely, SP-A and SP-B, in a rat model. Sprague–Dawley rats were exposed to cigarette smoke in a nose-only exposure system twice a day, every day for 70 weeks. At termination, bronchoalveolar lavage (BAL) fluid and the lung tissues were collected from room control, sham-treated (SH), and smoke-exposed (SM) animals for analyses. The total protein levels in the BAL fluid of SM rats tended to be higher but were not statistically different from those of the SH group. However, the albumin content of BAL fluid in SM rats, measured by quantitative immunoblotting, was significantly higher than in control groups. Compared to control groups, SP-A and SP-B levels in the BAL fluid of SM rats were significantly reduced by 25 and 50%, respectively, when expressed as units per microgram of BAL fluid protein. However, when calculated as total BAL fluid SP recovered per rat, only the SP-B levels of SM rats were significantly different from the control groups. Further analysis by ELISA confirmed the reduced levels of SP-B in SM rats. In contrast to BAL fluid, the lung tissue levels of SP and their respective mRNAs were not significantly different between the control and smoke-exposed groups. These results show a selective reduction in SP-B content on the bronchoalveolar surface following chronic exposure to cigarette smoke and suggest an inhibitory effect of cigarette smoke on surfactant secretory processes and/or a localized destruction of SPs on the bronchoalveolar surface.