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作 者:王伟[1] 罗向阳[1] 蔡丽霞[1] 崔志瑞[1]
出 处:《医药论坛杂志》2014年第8期12-14,共3页Journal of Medical Forum
基 金:河南省卫生科技创新型人才工程专项资助(201052);河南省医学科技攻关计划项目(201303092)
摘 要:目的观察宫内炎性暴露对早产大鼠支气管肺泡灌洗液内血管内皮生长因子及其受体含量的影响,探讨其与新型支气管肺发育不良发病机制之间的关系。方法定期受孕的Sprague Dawley(SD)大鼠随机分为脂多糖(LPS)组和生理盐水组(对照组),于孕15d羊膜腔内注射LPS/无菌生理盐水。两组动物均于出生后第1d(P1)、3d(P3)、5d(P5)和7d(P7)各随机取8只,应用ELISA方法检测BALF中VEGF及其受体的含量。结果LPS组随鼠龄递增,VEGF含量逐渐增加,P7达高峰。与对照组相比,LPS组在P1显著低于对照组(P<0.05);在P5明显高于对照组,并且差异有统计学意义(P<0.05)。其受体Flk-1的含量变化规律与其基本类似。结论宫内炎性暴露可通过调控VEGF及其受体的含量,引起肺微血管发生病理性重塑,肺泡化过程受阻,进而导致BPD的发生。Objective To investigate the levels of vascular endothelial growth factor(VEGF) and its receptor fetal liver kinase- 1(Flk- 1)in bronchoalveolar lavage fluid(BALF) of preterm rats lungs exposed to intra- amniotic endotoxin and to elucidate the relationship between intrauterine inflammatory exposure and the pathogenesis of BPD. Methods Timed pregnant Sprague Dawley(SD) rats were randomly divided into two groups: saline group and LPS group. LPS or saline were intra- amniotic injected into the bows on gestational age day 15(70% of term),respectively. The lungs from groups aged postnatal day 1(P1),3(P3),5(P5) and 7(P7) were removed and dissected from the main bronchi for analysis. Eight rats of each group were used to assess VEGF and its receptor levels with ELISA. Results VEGF and Flk- 1 levels increased along with the lung development from P1 to P7 in the control group. Compared with the contral group,VEGF and Flk- 1 levels in LPS group were lower than controls on P1(P 〈0. 05),and higher than controls on P7(P〈 0. 05). Conclusion These results suggest the intra- amniotic endotoxin can down- regulate of VEGF and Flk- 1,which may contribute to the pathophysiology of BPD.
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