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[博来霉素损伤的大鼠肺泡Ⅱ型细胞]

[Rat alveolar type II injured by bleomycin].

作者信息

Kong Lu, Wang Zhi-gang, Niu Jian-zhao, Wang Ji-feng, Jin Huan, Yang Mei-juan, Wang Ling-qiao, Tang Bing-hua, Zhang Qiu-ju, Tu Heng-jing

机构信息

Laboratory of Cell Biochemistry, Beijing University of Chinese Medicine, Beijing 100029, China.

出版信息

Zhongguo Yi Xue Ke Xue Yuan Xue Bao. 2005 Feb;27(1):81-6.

Abstract

OBJECTIVE

To explore dysfunction mechanism of rat alveolar type II (AT-II) injured by bleomycin (BLM).

METHODS

SD rats were injected with a single intratracheal dose of bleomycin or control saline. On day 7, 14, and 28 following intratracheal bleomycin or saline instillation, animals were killed under overdose of 1.5% sodium pentobarbital (0.25 ml/100 g, i.p.) and bronchoalveolar lavage fluid (BALF) from the lung was tested for the activity of pulmonary surfactant (PS) by the Whihelmy Film Balance. Several concentrations of bleomycin stimulated the culture of rat AT-II cells, and surfactant protein (SP) A, B, and aquaporin-1 (AQP) mRNA were analyzed by fluorescent quantitative polymerase chain reaction (FQ-PCR).

RESULTS

The activity of PS and hypoxemia significantly decreased on day 7 and improved on day 14 and completely recovered to normal status on day 28. SP-A, B, and AQP-1 mRNA expression in BLM-stimulated group were significantly lower than those in the control group (P<0.001).

CONCLUSION

BLM-injured AT-II cells decrease the levels of SP-A, B, and AQP-1 mRNA and cause PS dysfunction, resulting in hypoxemia and pneumonedema.

摘要

目的

探讨博来霉素(BLM)致大鼠Ⅱ型肺泡上皮细胞(AT-II)损伤的功能障碍机制。

方法

将博来霉素或对照生理盐水经气管内单次注入SD大鼠体内。在气管内注入博来霉素或生理盐水后的第7天、14天和28天,动物在过量给予1.5%戊巴比妥钠(0.25 ml/100 g,腹腔注射)麻醉下处死,用威尔赫姆薄膜天平检测肺支气管肺泡灌洗液(BALF)中肺表面活性物质(PS)的活性。用几种浓度的博来霉素刺激大鼠AT-II细胞培养,通过荧光定量聚合酶链反应(FQ-PCR)分析表面活性蛋白(SP)A、B和水通道蛋白-1(AQP)mRNA。

结果

PS活性和低氧血症在第7天显著降低,第14天有所改善,第28天完全恢复至正常状态。博来霉素刺激组的SP-A、B和AQP-1 mRNA表达显著低于对照组(P<0.001)。

结论

博来霉素损伤的AT-II细胞降低了SP-A、B和AQP-1 mRNA水平,导致PS功能障碍,进而引起低氧血症和肺水肿。

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