Cardioprotective Effects of Qishenyiqi Mediated by Angiotensin II Type 1 Receptor Blockade and Enhancing Angiotensin-Converting Enzyme 2.

Cardioprotective Effects of Qishenyiqi Mediated by Angiotensin II Type 1 Receptor Blockade and Enhancing Angiotensin-Converting Enzyme 2.
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DOI:
10.1155/2012/978127
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发表时间:
2012
期刊:
Evidence-based complementary and alternative medicine : eCAM
影响因子:
--
通讯作者:
Wang W
Wang W
中科院分区:
其他
文献类型:
--
作者:
Wang Y;Li C;Ouyang Y;Yu J;Guo S;Liu Z;Li D;Han J;Wang W

文献摘要

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本文的目的是探讨QSYQ对冠心病的影响是否与肾素-血管紧张素-醛固酮系统(RAAS)有关。配方组以福辛普利钠为对照,用QSYQ灌洗。分别测定心肌组织中RAAS组分的水平。结果表明,QSYQ和fosinopril钠均能提高冠心病患者的射血分数,QSYQ能降低左室收缩末内径和左室舒张末内径,而fosinopril钠对上述参数无影响。福辛普利钠作为ACE抑制剂,可下调ACE表达,最终降低组织AngII浓度,但对ACE2无影响。此外,对肾素和AT2无影响,而QSYQ可显著降低心肌组织肾素水平和AngII表达。QSYQ可同时作用于AT1和AT2,从而阻断AngII的作用,提高ACE2的水平。下调TGF-β和MMP-9水平,但对ACE无影响。本研究表明,芪syq对大鼠冠心病的改善作用具有多个与抑制RAAS相关的靶点,从而产生保护心脏的治疗作用。
The aim of this paper was to investigate whether the effects of QSYQ on CHD are associated with the renin-angiotensin-aldosterone system (RAAS). The formula groups were lavaged with QSYQ, using fosinopril sodium as a control. The level of RAAS components in the myocardial tissue was measured, respectively. The results showed that both QSYQ and fosinopril sodium can improve the ejection fraction in CHD and that QSYQ decreases the left ventricular end-systolic diameter and left ventricular end-diastolic diameter, while fosinopril sodium has no effects on these parameters. Fosinopril sodium, as an ACE inhibitor, downregulated ACE expression and eventually reduced the tissue AngII concentration but had no effect on ACE2. Moreover, it had no effect on renin or AT2, while QSYQ significantly decreased the level of renin and expression of AngII in myocardial tissue. The results also revealed that QSYQ can act on both AT1 and AT2, thus, blocking the effect of AngII and increasing the level of ACE2. It also downregulated the levels of TGF-β and MMP-9, but it had no effect on ACE. This study showed that the ameliorative effects of QSYQ on CHD in rats had multiple targets associated with the inhibition of RAAS, thus, producing cardioprotective therapy effects.