PI3K/Akt信号通路在缺氧性肺血管收缩中的机制 |
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引用本文: | 王丽荣,李爽,袁辉,李姝,董凯,张春军,吴红.PI3K/Akt信号通路在缺氧性肺血管收缩中的机制[J].牡丹江医学院学报,2010,31(3):7-9. |
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作者姓名: | 王丽荣 李爽 袁辉 李姝 董凯 张春军 吴红 |
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作者单位: | 1. 牡丹江医药有限公司,黑龙江,牡丹江,157000 2. 牡丹江医学院,黑龙江,牡丹江,157000 |
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基金项目: | 黑龙江省自然科学基金,黑龙江省卫生厅科研项目 |
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摘 要: | 目的:探讨15-羟基二十碳四烯酸(15-HETE)致大鼠肺动脉收缩的信号转导途径,阐明15-HETE引起慢性缺氧性肺动脉收缩作用的可能机制。方法:采用组织浴槽血管环方法观察15-HETE对缺氧和正常组大鼠血管收缩的作用,同时观察PI3K/Akt抑制剂LY294002对肺动脉环收缩强度的改变,明确PI3K/Akt信号转导途径在15-HETE收缩肺动脉中的作用。结果:15-HETE对正常组和缺氧模型组大鼠血管环均有收缩作用,加入AKT抑制剂LY294002可明显阻断15-HETE对缺氧大鼠肺动脉的收缩作用(P〈0.05)。结论:15-HETE通过AKT信号转导途径收缩慢性缺氧性大鼠肺动脉。
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关 键 词: | 缺氧性肺血管收缩 15-羟基二十碳四烯酸 AKT LY294002 肺动脉环 |
THE MECHANISM OF PI3K/AKT SIGNALING PATHWAY IN HYPOXIC PULMONARY VASOCONSTRICTION |
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Institution: | Wang Lirong et al(Mudanjiang Medical Co.,Ltd.Mudanjiang Heilongjiang 157000) |
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Abstract: | Objective:The aim of the present study was to investigate whether PI3K/Akt involved in 15-hydroxyeicosatetraenoic acid(15-HETE)-induced chronic hypoxic pulmonary artery(PA) constriction and clarified the mechanism of hypoxic pulmonary vas oconstriction(HPV).Methods:Pulmonary arterial rings were used to assess the role of 15-HETE in pulmonary artery tension from hypoxic and normoxic rats,furthermore,the inhibitor of PI3K/Akt signaling pathway was employed to determine the role of PI3K/Akt signaling pathway in 15-HETE induced pulmonary vasoconstriction.Results:15-HETE constricted the pulmonary artery rings of both hypoxic and nomorxic rats;and LY294002 reduced 15-HETE vasoconstriction effect significantly(P〈0.05).Conclusion:15-HETE constricts the pulmonary arteries of rats in chronic hypoxia via PI3K/Akt signaling pathway. |
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Keywords: | AKT LY294002 |
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