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埃他卡林对低氧诱导的肺动脉高压大鼠炎症反应的影响

吴苏玲 解卫平 孔辉 毕立清 朱蓉

南京医科大学学报(自然科学版)2013,Vol.33Issue(2):149-154,6.
南京医科大学学报(自然科学版)2013,Vol.33Issue(2):149-154,6.DOI:10.7655/NYDXBNS20130201

埃他卡林对低氧诱导的肺动脉高压大鼠炎症反应的影响

Effects of iptakalim on inflammation in hypoxia-induced pulmonary artery hypertension in rats

吴苏玲 1解卫平 1孔辉 1毕立清 1朱蓉1

作者信息

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摘要

Abstract

Objective:To investigate the effects of iptakalim(IPT),an adenosine triphosphate(ATP)-sensitive potassium channel opener,on the inflammation of hypoxic pulmonary artery hypertension(HPAH) in rats. Methods; A total of 96 SD rats were randomly divided into three groups(the control group,the hypoxia group and the hypoxia + IPT group,n=32 for each group). Hypoxia-treated and IPT-treated rats were placed into normobaric hypoxia chamber for 4 weeks(8 h/day,6 days/week). Eight rats of each group were killed at the end of each week. The right ventricle systolic pressure (RVSP) was measured and the small pulmonary arterial morphologic changes were detected by HE staining. Enzyme-linked immunosorbent assay (ELISA) was performed to analy2e the content of interleukin-lβ(IL-1β) and IL-10. Immunohistochemisty for ED1+ monocytes was performed to detect inflammatory cells around pulmonary arterioles. Results;IPT significantly inhibited RVSP increasing induced by hypoxia the remodeling of small pulmonary artery wall and the infiltrating of the arounding inflammatory cells. Moreover,IPT prevented IL-1β increasing and IL-10 decreasing induced by hypoxia in both peripheral blood and lung. Conclusion;IPT can alleviate inflammation in pulmonary vascular, lower the RVSP,antagonize the proliferation and remodeling of the small pulmonary artery. It is a promising candidate for the treatment of HPAH.

关键词

ATP敏感性钾通道/埃他卡林/炎症反应/低氧性肺动脉高压

Key words

KATP channel/ iptakalim/ inflammation/ hypoxic pulmonary artery hypertension

分类

医药卫生

引用本文复制引用

吴苏玲,解卫平,孔辉,毕立清,朱蓉..埃他卡林对低氧诱导的肺动脉高压大鼠炎症反应的影响[J].南京医科大学学报(自然科学版),2013,33(2):149-154,6.

基金项目

国家自然科学基金(81273571) (81273571)

江苏省人事厅六大人才高峰资助项目(2008074) (2008074)

南京医科大学学报(自然科学版)

OA北大核心CSCDCSTPCD

1007-4368

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