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

Wang Y, Li C, Ouyang Y, Yu J, Guo S, Liu Z, Li D, Han J, Wang W - Evid Based Complement Alternat Med (2012)

Bottom Line: 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.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.

View Article: PubMed Central - PubMed

Affiliation: Beijing University of Chinese Medicine, Bei San Huan Dong Lu 11, Chao Yang District, Beijing 100029, China.

ABSTRACT
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.

No MeSH data available.


Related in: MedlinePlus

QSYQ significantly decreased cardiac renin and AT1 and increased AT2 in rats with CHD. Data were analyzed by one-way ANOVA, with P < 0.05 indicating statistical significance. *Differed significantly from the model group (P < 0.05).
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fig4: QSYQ significantly decreased cardiac renin and AT1 and increased AT2 in rats with CHD. Data were analyzed by one-way ANOVA, with P < 0.05 indicating statistical significance. *Differed significantly from the model group (P < 0.05).

Mentions: Western blot analysis of renin showed that at the end of the study, the cardiac renin in the model group (1.41 ± 0.292) increased compared with that in the sham-operated group (1.00 ± 0.000, P < 0.05). After treatment with fosinopril sodium (1.16 ± 0.087), the renin concentration was not significantly different between the groups; after treatment with QSYQ for 28 days, the level of renin (0.92 ± 0.154, P < 0.05) showed a 22.76% reduction compared with the model group, which had no statistical significance compared with the sham group (Figure 4).


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

Wang Y, Li C, Ouyang Y, Yu J, Guo S, Liu Z, Li D, Han J, Wang W - Evid Based Complement Alternat Med (2012)

QSYQ significantly decreased cardiac renin and AT1 and increased AT2 in rats with CHD. Data were analyzed by one-way ANOVA, with P < 0.05 indicating statistical significance. *Differed significantly from the model group (P < 0.05).
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3526154&req=5

fig4: QSYQ significantly decreased cardiac renin and AT1 and increased AT2 in rats with CHD. Data were analyzed by one-way ANOVA, with P < 0.05 indicating statistical significance. *Differed significantly from the model group (P < 0.05).
Mentions: Western blot analysis of renin showed that at the end of the study, the cardiac renin in the model group (1.41 ± 0.292) increased compared with that in the sham-operated group (1.00 ± 0.000, P < 0.05). After treatment with fosinopril sodium (1.16 ± 0.087), the renin concentration was not significantly different between the groups; after treatment with QSYQ for 28 days, the level of renin (0.92 ± 0.154, P < 0.05) showed a 22.76% reduction compared with the model group, which had no statistical significance compared with the sham group (Figure 4).

Bottom Line: 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.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.

View Article: PubMed Central - PubMed

Affiliation: Beijing University of Chinese Medicine, Bei San Huan Dong Lu 11, Chao Yang District, Beijing 100029, China.

ABSTRACT
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.

No MeSH data available.


Related in: MedlinePlus