發(fā)布時(shí)間：2018-04-06 23:33

  本文選題：松齡血脈康　切入點(diǎn)：高血壓　出處：《中國(guó)中醫(yī)基礎(chǔ)醫(yī)學(xué)雜志》2017年05期

【摘要】：目的::探討松齡血脈康對(duì)自發(fā)性高血壓大鼠血壓的干預(yù)作用及機(jī)制。方法:自發(fā)性高血壓大鼠隨機(jī)分組后分別灌胃給予松齡血脈康和氯沙坦鉀,連續(xù)給藥9周,每周檢測(cè)收縮壓、舒張壓變化。以HE染色觀察藥物對(duì)大鼠主動(dòng)脈病理組織形態(tài)學(xué)影響,qPCR陣列技術(shù)檢測(cè)高血壓相關(guān)因子RNA水平的變化,繼而借助String及KEGG Pathway數(shù)據(jù)庫(kù)對(duì)差異基因進(jìn)行網(wǎng)絡(luò)分析。結(jié)果:給藥9周后,與模型組比較高劑量松齡血脈康組及氯沙坦鉀組大鼠的收縮壓、舒張壓均顯著降低;高劑量松齡血脈康組大鼠血漿中血管緊張素Ⅱ水平較模型組明顯降低,且與氯沙坦組比較特別顯著性降低;對(duì)qPCR篩選得到的12個(gè)差異表達(dá)基因進(jìn)行網(wǎng)絡(luò)分析發(fā)現(xiàn),Pde5a、Prkg1、Gucy1b3和Prkg2相互作用明顯,且均參與cGMP-PKG通路的活化。結(jié)論:松齡血脈康降低自發(fā)性高血壓大鼠血壓,其機(jī)制可能與降低大鼠血漿中AngⅡ水平、調(diào)控差異表達(dá)基因Pde5a、Prkg1、Gucy1b3和Prkg2共同參與的c GMP-PKG通路有關(guān)。
[Abstract]:Objective: to investigate the effect and mechanism of Songling Xuemaikang on blood pressure in spontaneously hypertensive rats.Methods: spontaneously hypertensive rats were randomly divided into two groups: Songling Xuemaikang and Losartan potassium were given orally for 9 weeks. Systolic blood pressure and diastolic blood pressure were measured every week.The effect of drugs on the pathological morphology of rat aorta was observed by HE staining. The changes of RNA level of hypertension related factors were detected by qPCR array technique, and then the differential genes were analyzed by String and KEGG Pathway database.Results: after 9 weeks of administration, compared with the model group, the systolic and diastolic blood pressure of the rats in the high dose Songling Xuemaikang group and the losartan potassium group were significantly decreased, and the plasma angiotensin 鈪，

本文編號(hào)：1719430