本文選題：Forskolin　切入點：C型鈉尿肽　出處：《延邊大學(xué)》2017年碩士論文

【摘要】：目的:觀察C型鈉尿肽(C-type natriuretic peptid,CNP)對缺氧心房的機(jī)械活動及其缺氧誘導(dǎo)因子-1a(hypoxia-inducible factor-1a,HIF-1a)活性的影響,并探討腺苷酸環(huán)化酶激活劑Forskolin對CNP調(diào)節(jié)缺氧心房機(jī)械活動及HIF-1a活性的作用。方法:本研究利用SD大鼠為實驗對象,制備離體搏動的急性缺氧大鼠心房灌流裝置模型。實驗分為對照組、缺氧組、缺氧加CNP組、缺氧加Forskolin組、缺氧加CNP組加Forskolin組。運(yùn)用生物記錄儀監(jiān)測心房搏動壓的變化,運(yùn)用蛋白印跡技術(shù)(western blot,WB)的方法,檢測磷酸二酯酶3A亞型(phosphodiesterse type 3A,PDE 3A)和 HIF-1a 的表達(dá)。結(jié)果:1.缺氧明顯抑制心房搏動壓,CNP則易化缺氧抑制心房機(jī)械活動的效應(yīng)。2.Forskolin明顯減緩CNP抑制缺氧心房機(jī)械活動的作用,但Forskolin未能改變單純?nèi)毖跻种菩姆繖C(jī)械活動的效應(yīng)。3.Forskolin明顯增加缺氧心房肌組織PDE 3A含量。缺氧及CNP均未能改變?nèi)毖跣姆縋DE 3A的含量,但在Forskolin存在下CNP顯著降低PDE 3A的含量。4.缺氧明顯著增加心房肌組織HIF-1a含量,Forskolin則增強(qiáng)缺氧增加心房肌組織HIF-1a含量的作用;而CNP不僅可完全阻斷缺氧增加心房肌組織HIF-1a含量的作用,而且明顯抑制Forskolin對缺氧心房HIF-1a含量的效應(yīng)。結(jié)論:1.CNP顯著抑制離體搏動大鼠缺氧心房的機(jī)械活動及其HIF-1其活性;2.Forskolin通過CNP-PDE3A信號通路明顯減緩CNP抑制心房機(jī)械活動及其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.
【學(xué)位授予單位】：延邊大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2017
【分類號】：R54
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本文編號：1654449