摘要
目的::探讨松龄血脉康对自发性高血压大鼠血压的干预作用及机制。方法:自发性高血压大鼠随机分组后分别灌胃给予松龄血脉康和氯沙坦钾,连续给药9周,每周检测收缩压、舒张压变化。以HE染色观察药物对大鼠主动脉病理组织形态学影响,qPCR阵列技术检测高血压相关因子RNA水平的变化,继而借助String及KEGG Pathway数据库对差异基因进行网络分析。结果:给药9周后,与模型组比较高剂量松龄血脉康组及氯沙坦钾组大鼠的收缩压、舒张压均显著降低;高剂量松龄血脉康组大鼠血浆中血管紧张素Ⅱ水平较模型组明显降低,且与氯沙坦组比较特别显著性降低;对qPCR筛选得到的12个差异表达基因进行网络分析发现,Pde5a、Prkg1、Gucy1b3和Prkg2相互作用明显,且均参与cGMP-PKG通路的活化。结论:松龄血脉康降低自发性高血压大鼠血压,其机制可能与降低大鼠血浆中AngⅡ水平、调控差异表达基因Pde5a、Prkg1、Gucy1b3和Prkg2共同参与的c GMP-PKG通路有关。
Objective: To investigate the mechanism of Songling Xnemaikang Capsule (SXC) on blood pressure of spontaneously hypertensive rats (SHR). Methods: SHR were randomly divided into model group, high dose SXC group (H-SXC) , normal dose SXC group(N-SXC) and losartan group. Blood pressures were measured every week. Pathological morphology of aorta was observed by HE staining. String and KEGG Pathway databases were used for network analysis of differentially expressed genes which related with hypertension and detected with qPCR arrays. Results: Compared with model group, bood pressure of H-SXC and losartan group decreased significantly after 9 weeks of irrigation. AngiotensinⅡ level declined obviously compared with model group and even losartan group. 12 differentially expressed genes were screened by qPCR arrays and among which 4 genes including PdeSa, Prkgl, Gucylb3 and Prkg2 participated in cGMP- PKG pathway. Conclusion: SXC could decrease increased blood pressure of SHR, the regulatory mechanism of which might be due to angiotensin Ⅱ , and the involvement of cGMP-PKG pathway.
出处
《中国中医基础医学杂志》
CSCD
北大核心
2017年第5期634-637,671,共5页
JOURNAL OF BASIC CHINESE MEDICINE
基金
北京市"十病十药"研发专项(Z141100002214011)-气血并治颗粒的制剂开发研究