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. 2012:2012:795452.
doi: 10.1155/2012/795452. Epub 2012 Feb 9.

VSports在线直播 - Beneficial effects of long-term administration of an oral formulation of Angiotensin-(1-7) in infarcted rats

Fúlvia D Marques  1 , Marcos B Melo, Leandro E Souza, Maria Claúdia C Irigoyen, Rúben D Sinisterra, Frederico B de Sousa, Sílvia Q Savergnini, Vinícius B A Braga, Anderson J Ferreira, Robson A S Santos
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Beneficial effects of long-term administration of an oral formulation of Angiotensin-(1-7) in infarcted rats

Fúlvia D Marques et al. Int J Hypertens. 2012.

"V体育安卓版" Abstract

In this study was evaluated the chronic cardiac effects of a formulation developed by including angiotensin(Ang)-(1-7) in hydroxypropyl β-cyclodextrin (HPβCD), in infarcted rats. Myocardial infarction (MI) was induced by left coronary artery occlusion. HPβCD/Ang-(1-7) was administered for 60 days (76 μg/Kg/once a day/gavage) starting immediately before infarction. Echocardiography was utilized to evaluate usual cardiac parameters, and radial strain method was used to analyze the velocity and displacement of myocardial fibers at initial time and 15, 30, and 50 days after surgery VSports手机版. Real-time PCR was utilized to evaluate the fibrotic signaling involved in the remodeling process. Once-a-day oral HPβCD/Ang-(1-7) administration improved the cardiac function and reduced the deleterious effects induced by MI on TGF-β and collagen type I expression, as well as on the velocity and displacement of myocardial fibers. These findings confirm cardioprotective effects of Ang-(1-7) and indicate HPβCD/Ang-(1-7) as a feasible formulation for long-term oral administration of this heptapeptide. .

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Figures

Figure 1
Figure 1
Effects of HPβCD/Ang-(1–7) on echocardiographic parameters after left coronary artery ligation in rats followed for up to 50 days. (a) Fractional shortening, (b) ejection fraction, (c) end systolic left ventricular volume, (d) end diastolic left ventricular volume, (e) interventricular septal dimension in systole, and (f) interventricular septal dimension in diastole. *P < 0.05  versus sham; **P < 0.01  versus sham; ***P < 0.001 versus sham; † P < 0.05 versus MI (two-way ANOVA followed by the Bonferroni posttest).
Figure 2
Figure 2
Representative M-mode images showing cardiac function and left ventricle chamber dimensions in sham, MI, and MI + HPβCD/Ang-(1–7)-treated rats. Note the marked increase in end-systolic dimension (ESD) and in end-diastolic dimension (EDD) after infarction and the improvement in the cardiac function after 50 days in rats treated with HPβCD/Ang-(1–7).
Figure 3
Figure 3
Effects of HPβCD/Ang-(1–7) on the variation of the velocity and displacement in rats after (a and b) 15 days; (c and d) 30 days, and (e and f) 50 days of treatment. *P < 0.05 versus sham; † P < 0.05 versus MI; ‡ P < 0.01 versus MI (one-way ANOVA followed by the Newman-Keuls posttest).
Figure 4
Figure 4
Representative images of the radial strain analysis of the velocity (cm/s) at basal conditions and after 15 and 50 days of MI. (a) sham group, (b) MI group, and (c) MI + HPβCD/Ang-(1–7).
Figure 5
Figure 5
Representative images of radial strain analysis of the displacement (mm) at basal conditions and after 15 and 50 days of MI. (a) sham group, (b) MI group, and (c) MI + HPβCD/Ang-(1–7).
Figure 6
Figure 6
Effects of long-term administration of HPβCD/Ang-(1–7) on mRNA expression of (a) TGF-β, (b) collagen type I, and (c) Mas in infarcted animals. *P < 0.05 and **P < 0.01 versus sham; † P < 0.01 versus MI (one-way ANOVA followed by the Newman-Keuls posttest) (a.u) = Arbitrary Units.
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