Cardiac Contractile Dysfunction and Apoptosis in Streptozotocin-Induced Diabetic Rats Are Ameliorated by Garlic Oil Supplementation

Department of Physical Therapy and Graduate Institute of Rehabilitation Science, China Medical University, 91 Hsueh-ShihRoad, Taichung 404, Taiwan.
Journal of Agricultural and Food Chemistry (Impact Factor: 2.91). 10/2010; 58(19):10347-55. DOI: 10.1021/jf101606s
Source: PubMed


Previous studies have suggested that garlic oil could protect the cardiovascular system. However, the mechanism by which garlic oil protects diabetes-induced cardiomyopathy is unclear. In this study, streptozotocin (STZ)-induced diabetic rats received garlic oil (0, 10, 50, or 100 mg/kg of body weight) by gastric gavage every 2 days for 16 days. Normal rats without diabetes were used as control. Cardiac contractile dysfunction examined by echocardiography and apoptosis evaluated by terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) assay were observed in diabetic rat hearts. Additionally, a shift in cardiac myosin heavy chain (MHC) gene expression from α- to β-MHC isoform, decreased levels of superoxide dismutase-1 (SOD-1) and cardiac α-actin, and elevated cardiac thiobarbituric acid reactive substances (TBARS) and caspase- and p38-NFκB-leading apoptosis signaling activities were demonstrated in diabetic hearts. However, these diabetes-related cardiac dysfunctions were almost dose-dependently ameliorated by garlic oil administration. In conclusion, garlic oil possesses significant potential for protecting hearts from diabetes-induced cardiomyopathy.

Download full-text


Available from: Stephen Tzang, Dec 21, 2013
22 Reads
  • Source
    • "In our database, one study showed that transcript levels of cardiac α-actin did not change in STZ-induced rats [14]. Two studies showed that cardiac α-actin was reduced in STZ-induced diabetic rats [72] and db/db type 2 diabetic mice [73]. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Pathological cardiac hypertrophy activates a suite of genes called the fetal gene program (FGP). Pathological hypertrophy occurs in diabetic cardiomyopathy (DCM); therefore, the FGP is widely used as a biomarker of DCM in animal studies. However, it is unknown whether the FGP is a consistent marker of hypertrophy in rodent models of diabetes. Therefore, we analyzed this relationship in 94 systematically selected studies. Results showed that diabetes induced with cytotoxic glucose analogs such as streptozotocin was associated with decreased cardiac weight, but genetic or diet-induced models of diabetes were significantly more likely to show cardiac hypertrophy (P<0.05). Animal strain, sex, age, and duration of diabetes did not moderate this effect. There were no correlations between the heart weight:body weight index and mRNA or protein levels of the fetal genes α-myosin heavy chain (α-MHC) or β-MHC, sarco/endoplasmic reticulum Ca2+-ATPase, atrial natriuretic peptide (ANP), or brain natriuretic peptide. The only correlates of non-indexed heart weight were the protein levels of α-MHC (Spearman's ρ = 1, P<0.05) and ANP (ρ = -0.73, P<0.05). These results indicate that most commonly measured genes in the FGP are confounded by diabetogenic methods, and are not associated with cardiac hypertrophy in rodent models of diabetes.
    PLoS ONE 03/2014; 9(3):e92903. DOI:10.1371/journal.pone.0092903 · 3.23 Impact Factor
  • Source
    • "The relationship between diabetic cardiomyopathy and cellular apoptosis is well known [45,59-61]. Previous studies demonstrate IMD administration decreases MI/R-induced cardiomyocyte apoptosis [11,17], and myocardial injury may be exacerbated by downregulated IMD during early reperfusion [62]. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Background Diabetic patients, through incompletely understood mechanisms, endure exacerbated ischemic heart injury compared to non-diabetic patients. Intermedin (IMD) is a novel calcitonin gene-related peptide (CGRP) superfamily member with established cardiovascular protective effects. However, whether IMD protects against diabetic myocardial ischemia/reperfusion (MI/R) injury is unknown. Methods Diabetes was induced by streptozotocin in Sprague–Dawley rats. Animals were subjected to MI via left circumflex artery ligation for 30 minutes followed by 2 hours R. IMD was administered formally 10 minutes before R. Outcome measures included left ventricular function, oxidative stress, cellular death, infarct size, and inflammation. Results IMD levels were significantly decreased in diabetic rats compared to control animals. After MI/R, diabetic rats manifested elevated intermedin levels, both in plasma (64.95 ± 4.84 pmol/L, p < 0.05) and myocardial tissue (9.8 ± 0.60 pmol/L, p < 0.01) compared to pre-MI control values (43.62 ± 3.47 pmol/L and 4.4 ± 0.41). IMD administration to diabetic rats subjected to MI/R decreased oxidative stress product generation, apoptosis, infarct size, and inflammatory cytokine release (p < 0.05 or p < 0.01). Conclusions By reducing oxidative stress, inflammation, and apoptosis, IMD may represent a promising novel therapeutic target mitigating diabetic ischemic heart injury.
    Cardiovascular Diabetology 06/2013; 12(1):91. DOI:10.1186/1475-2840-12-91 · 4.02 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Garlic ( Allium sativum ) possesses anti-inflammatory effects. This study investigated the effects of garlic oil on endotoxin-induced neutrophil infiltration in the small intestine. Wistar rats received by gavage 10, 50, or 100 mg/kg body wt garlic oil (GO) or the vehicle (corn oil; 2 mL/kg body wt) every other day for 2 weeks before being injected with endotoxin (ip, 5 mg/kg body wt). Control rats were administered corn oil and injected with sterile saline. Blood samples for the measurement of soluble adhesion molecules were collected at various time points after injection, and all other samples were collected 18 h after injection. The 10 and 50 mg/kg doses suppressed endotoxin-induced neutrophilia, serum levels of sL-selectin and sICAM-1, cellular CD11b on neutrophils, intestinal ICAM-1 content, and neutrophil infiltration (P < 0.05). The 100 mg/kg dose significantly lowered local ICAM-1 and cellular CD11b on neutrophils (P < 0.05) but did not have a beneficial effect on neutrophil infiltration. In addition, 100 mg/kg of GO worsened the elevation of the local TNF-α level and neutrophilia. Appropriate doses of garlic oil have a preventive effect on endotoxin-induced neutrophil infiltration and damage to the small intestine.
    Journal of Agricultural and Food Chemistry 06/2011; 59(14):7717-25. DOI:10.1021/jf201185v · 2.91 Impact Factor
Show more