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[高浓度氧长时间暴露对新生大鼠肺组织血管内皮生长因子及其受体表达的影响]

[Effects of prolonged exposure of high concentration of oxygen on expression of vascular endothelial growth factor and its receptors in neonatal rat lungs].

作者信息

Feng Hai-Yan, Lu Ai-Zhen, Zhang Xiao-Bo, Wang Li-Bo, Chen Chao

机构信息

Children's Hospital of Fudan University, Shanghai 201102, China.

出版信息

Zhongguo Dang Dai Er Ke Za Zhi. 2009 Nov;11(11):927-30.

Abstract

OBJECTIVE

To study the effects of prolonged 75% oxygen exposure on the expression of vascular endothelial growth factor (VEGF) and its receptors (VEGFR1 and VEGFR2) in the neonatal rat lungs and to elucidate the effects of prolonged exposure of high concentration of oxygen on lung vascular development and its relationship with bronchopulmonary dysplasia (BPD).

METHODS

Forty eight Sprague-Dawley rat pups were randomly exposed to air (control group) and 75% oxygen (experimental group) 12 hrs after birth. The rats were sacrificed 7, 14 and 21 days after exposure and their lungs were sampled. The lung sections were stained with hematoxylin and eosin for histological evaluation. Expression of VEGF, VEGFR1 and VEGFR2 protein and mRNA was detected by immunohistochemistry and RT-PCR.

RESULTS

After being exposed to 75% oxygen for 21 days, lung tissues had pathological changes as 'new' BPD. Expressions of VEGF protein (10.9 + or - 2.7 vs 30.8 + or - 6.4), VEGFR1 protein (5.4 + or - 1.4 vs 15.6 + or - 3.4) and VEGFR2 protein (11.3 + or - 2.6 vs 21.7 + or - 4.5) on day 21 in the experimental group decreased significantly as compared with the control group (p<0.05). The expression of VEGF mRNA (1.6 vs 3.3), VEGFR1 mRNA (0.4 vs 6.6) and VEGFR2 mRNA (0.5 vs 4.9) on day 21 in the experimental group also decreased significantly as compared with the control group (p<0.05).

CONCLUSIONS

Prolonged exposure of high concentration of oxygen may cause BPD possibly by inhibiting lung vascular development in neonatal rats.

摘要

目的

研究新生大鼠长时间暴露于75%氧气环境对血管内皮生长因子(VEGF)及其受体(VEGFR1和VEGFR2)表达的影响,以阐明高浓度氧气长时间暴露对肺血管发育的影响及其与支气管肺发育不良(BPD)的关系。

方法

48只Sprague-Dawley新生大鼠幼崽出生后12小时随机分为空气暴露组(对照组)和75%氧气暴露组(实验组)。暴露后7天、14天和21天处死大鼠并取肺组织。肺组织切片进行苏木精-伊红染色用于组织学评估。通过免疫组织化学和逆转录-聚合酶链反应检测VEGF、VEGFR1和VEGFR2蛋白及mRNA的表达。

结果

暴露于75%氧气21天后,肺组织出现类似“新”BPD的病理变化。实验组第21天时VEGF蛋白表达(10.9±2.7 vs 30.8±6.4)、VEGFR1蛋白表达(5.4±1.4 vs 15.6±3.4)和VEGFR2蛋白表达(11.3±2.6 vs 21.7±4.5)与对照组相比显著降低(p<0.05)。实验组第21天时VEGF mRNA表达(1.6 vs 3.3)、VEGFR1 mRNA表达(0.4 vs 6.6)和VEGFR2 mRNA表达(0.5 vs 4.9)与对照组相比也显著降低(p<0.05)。

结论

高浓度氧气长时间暴露可能通过抑制新生大鼠肺血管发育导致BPD。

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