Forskolin对CNP抑制缺氧心房机械活动及HIF-1a活性的影响

发布时间：2018-03-23 17:26

  本文选题：Forskolin　切入点：C型钠尿肽　出处：《延边大学》2017年硕士论文

【摘要】：目的:观察C型钠尿肽(C-type natriuretic peptid,CNP)对缺氧心房的机械活动及其缺氧诱导因子-1a(hypoxia-inducible factor-1a,HIF-1a)活性的影响,并探讨腺苷酸环化酶激活剂Forskolin对CNP调节缺氧心房机械活动及HIF-1a活性的作用。方法:本研究利用SD大鼠为实验对象,制备离体搏动的急性缺氧大鼠心房灌流装置模型。实验分为对照组、缺氧组、缺氧加CNP组、缺氧加Forskolin组、缺氧加CNP组加Forskolin组。运用生物记录仪监测心房搏动压的变化,运用蛋白印迹技术(western blot,WB)的方法,检测磷酸二酯酶3A亚型(phosphodiesterse type 3A,PDE 3A)和 HIF-1a 的表达。结果:1.缺氧明显抑制心房搏动压,CNP则易化缺氧抑制心房机械活动的效应。2.Forskolin明显减缓CNP抑制缺氧心房机械活动的作用,但Forskolin未能改变单纯缺氧抑制心房机械活动的效应。3.Forskolin明显增加缺氧心房肌组织PDE 3A含量。缺氧及CNP均未能改变缺氧心房PDE 3A的含量,但在Forskolin存在下CNP显著降低PDE 3A的含量。4.缺氧明显著增加心房肌组织HIF-1a含量,Forskolin则增强缺氧增加心房肌组织HIF-1a含量的作用;而CNP不仅可完全阻断缺氧增加心房肌组织HIF-1a含量的作用,而且明显抑制Forskolin对缺氧心房HIF-1a含量的效应。结论:1.CNP显著抑制离体搏动大鼠缺氧心房的机械活动及其HIF-1其活性;2.Forskolin通过CNP-PDE3A信号通路明显减缓CNP抑制心房机械活动及其HIF-1a活性的作用。
[Abstract]:Aim: to observe the effects of C-type natriuretic peptide C type natriuretic peptide on the mechanical activity of anoxic atrium and the activity of hypoxia-inducible factor-1a (HIF-1a). To investigate the effect of adenylate cyclase activator (Forskolin) on the regulation of hypoxic atrial mechanical activity and HIF-1a activity by CNP. Methods: SD rats were used as experimental subjects. The rat model of atrial perfusion was established in vitro. The rats were divided into control group, hypoxic group, hypoxia plus CNP group, hypoxia + Forskolin group, hypoxia + CNP group and Forskolin group. The changes of atrial pulsatile pressure were monitored by biological recorder. Using Western blotWBs, The expression of phosphodiesterse type 3AnPDE3A) and HIF-1a were detected. Results 1. The effect of hypoxia on inhibiting atrial mechanical activity was facilitated by hypoxia. 2. Forskolin significantly decreased the inhibitory effect of CNP on anoxic atrial mechanical activity. However, Forskolin did not change the effects of hypoxia alone on atrial mechanical activity. 3. Forskolin significantly increased the content of PDE 3A in hypoxic atrial myocytes. Hypoxia and CNP did not change the content of PDE 3A in anoxic atrium. However, in the presence of Forskolin, CNP significantly decreased the content of PDE 3A. 4. Hypoxia significantly increased the content of HIF-1a in atrial myocytes and forskolin enhanced the effect of hypoxia on the content of HIF-1a in atrial myocytes, while CNP not only completely blocked the effect of hypoxia on the increase of HIF-1a content in atrial myocytes. Conclusion: 1. CNP significantly inhibits the mechanical activity of isolated hypoxic rat atrium and its HIF-1 activity. 2. Forskolin significantly inhibits the inhibitory effect of CNP on atrial mechanical activity and HIF-1a activity through CNP-PDE3A signaling pathway.
【学位授予单位】：延边大学
【学位级别】：硕士
【学位授予年份】：2017
【分类号】：R54
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本文编号：1654449