Abstract

BackgroundOxidative stress plays a major role in diabetic cardiomyopathy pathogenesis. Anti-oxidant therapy has been investigated in preventing or treating several diabetic complications. However, anti-oxidant action on diabetic-induced cardiac remodeling is not completely clear. This study evaluated the effects of rutin, a flavonoid, on cardiac and myocardial function in diabetic rats.MethodsWistar rats were assigned into control (C, n = 14); control-rutin (C-R, n = 14); diabetes mellitus (DM, n = 16); and DM-rutin (DM-R, n = 16) groups. Seven days after inducing diabetes (streptozotocin, 60 mg/kg, i.p.), rutin was injected intraperitoneally once a week (50 mg/kg) for 7 weeks. Echocardiogram was performed and myocardial function assessed in left ventricular (LV) papillary muscles. Serum insulin concentration was measured by ELISA. Statistics: One-way ANOVA and Tukey’s post hoc test.ResultsGlycemia was higher in DM than DM-R and C and in DM-R than C-R. Insulin concentration was lower in diabetic groups than controls (C 2.45 ± 0.67; C-R 2.09 ± 0.52; DM 0.59 ± 0.18; DM-R 0.82 ± 0.21 ng/mL). Echocardiogram showed no differences between C-R and C. DM had increased LV systolic diameter compared to C, and increased left atrium diameter/body weight (BW) ratio and LV mass/BW ratio compared to C and DM-R. Septal wall thickness, LV diastolic diameter/BW ratio, and relative wall thickness were lower in DM-R than DM. Fractional shortening and posterior wall shortening velocity were lower in DM than C and DM-R. In papillary muscle preparation, DM and DM-R presented higher time to peak tension and time from peak tension to 50% relaxation than controls; time to peak tension was lower in DM-R than DM. Under 0.625 and 1.25 mM extracellular calcium concentrations, DM had higher developed tension than C.ConclusionRutin attenuates cardiac remodeling and left ventricular and myocardial dysfunction caused by streptozotocin-induced diabetes mellitus.

Highlights

  • Oxidative stress plays a major role in diabetic cardiomyopathy pathogenesis

  • At the end of the experiment, glycemia was statistically higher in diabetes mellitus group (DM) than DM-rutin group (DM-R) and C and in DM-R than control-rutin group (C-R) (C 98.9 ± 13.7; C-R 104 ± 11.9; DM 397 ± 57.5; DM-R 149 ± 30.3 mg/dL)

  • At the end of the study, serum insulin concentration was significantly lower in both diabetic groups compared to their respective controls (C 2.45 ± 0.67; C-R 2.09 ± 0.52; DM 0.59 ± 0.18; DM-R 0.82 ± 0.21 ng/mL)

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Summary

Introduction

Oxidative stress plays a major role in diabetic cardiomyopathy pathogenesis. Anti-oxidant therapy has been investigated in preventing or treating several diabetic complications. Anti-oxidant action on diabeticinduced cardiac remodeling is not completely clear. Cardiac alterations are caused by both coronary atherosclerosis and diabetes-related cardiomyopathy. As. Guimaraes et al Cardiovasc Diabetol (2015) 14:90 widely considered a major cause in the pathogenesis of diabetic cardiomyopathy [8,9,10]. Oxidative stress can be induced by hyperglycemia, hyperlipidemia, and inflammation. Anti-oxidant therapy has been extensively studied to prevent or treat several diabetic complications [12,13,14]; direct investigations on the role of anti-oxidants on diabetic-induced cardiac remodeling remain relatively scarce [9]

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