BackgroundTrimetazidine (TMZ) is an anti-ischemic drug. In spite of its protective
effects on cardiovascular system, there is no scientific study on the
usefulness of TMZ treatment for prolonged QT interval and cardiac
hypertrophy induced by diabetes.ObjectivesTo evaluate the effects of TMZ on QT interval prolongation and cardiac
hypertrophy in the diabetic rats.MethodsTwenty-four male Sprague-Dawley rats (200-250 g) were randomly assigned into
three groups (n = 8) by simple random sampling method. Control (C), diabetic
(D), and diabetic administrated with TMZ at 10 mg/kg (T10). TMZ was
administrated for 8 weeks. The echocardiogram was recorded before isolating
the hearts and transfer to a Langendorff apparatus. Hemodynamic parameters,
QT and corrected QT interval (QTc) intervals, heart rate and antioxidant
enzymes were measured. The hypertrophy index was calculated. The results
were evaluated by one-way ANOVA and paired t-test using SPSS (version 16)
and p < 0.05 was regarded as significant.ResultsThe diabetic rats significantly indicated increased hypertrophy, QT and QTc
intervals and decreased Left ventricular systolic pressure (LVSP), Left
ventricular developed pressure (LVDP), rate pressure product (RPP), Max
dp/dt, and min dp/dt (±dp/dt max), heart rate, superoxide dismutase
(SOD), glutathione peroxidase (GPx) and catalase in the heart. Treatment
with TMZ in the diabetic animals was significantly improved these parameters
in comparison to the untreated diabetic group.ConclusionsTMZ improves QTc interval prolongation and cardiac hypertrophy in diabetes.
Background Gallic acid (GA) is a polyphenolic agent with interesting pharmacological impacts on the cardiovascular system. Objective The present study purposed to study the protective effects of GA at 25 and 50 mg/kg against isoproterenol (ISO)-induced cardiac damage in ischemia/reperfusion (I/R) in rats. Methods Male Wistar rats were randomly assigned into six groups: Control, Control treated with GA at 25 mg/kg (GA25), Control treated with GA at 50 mg/kg (GA50), Hypertrophic rats induced by ISO (ISO), Hypertrophic rats treated with GA at 25 mg/kg (ISO+GA25), and Hypertrophic rats treated with GA at 50 mg/kg (ISO+GA50). Heart isolation was performed to induce a cardiac I/R injury model. Cardiac hemodynamic parameters were recorded. Serum Lactate Dehydrogenase (LDH) and Creatine Kinase-MB (CK-MB) and cardiac Superoxide dismutases (SOD) levels were evaluated. The gene expression of Sarcoplasmic reticulum Ca2+-ATPase (SERCA2a) was assessed. Results We found that GA at 50 mg/kg was significantly increased cardiac function at post I/R period in ISO-induced hypertrophic hearts. Moreover, it suppressed cardiac hypertrophy, the serum LDH and CK-MB levels in ISO injected rats. Administration of GA at 50 mg/kg was significantly increased SOD level and SERCA2a gene expression in the hypertrophic hearts. Conclusion GA at 50 mg/kg could improve cardiac performance possibly by increasing antioxidant defense enzymes, reducing cell damage, and enhancing SERCA2a gene expression in hypertrophic heart induced by ISO in I/R injury conditions.
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