RGD Reference Report - Multiple antioxidants improve cardiac complications and inhibit cardiac cell death in streptozotocin-induced diabetic rats. - Rat Genome Database

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Multiple antioxidants improve cardiac complications and inhibit cardiac cell death in streptozotocin-induced diabetic rats.

Authors: Kumar, S  Prasad, S  Sitasawad, SL 
Citation: Kumar S, etal., PLoS One. 2013 Jul 2;8(7):e67009. doi: 10.1371/journal.pone.0067009. Print 2013.
RGD ID: 7247697
Pubmed: PMID:23843977   (View Abstract at PubMed)
PMCID: PMC3699585   (View Article at PubMed Central)
DOI: DOI:10.1371/journal.pone.0067009   (Journal Full-text)

Diabetic cardiomyopathy, a disorder of the heart muscle in diabetic patients, is one of the major causes of heart failure. Since diabetic cardiomyopathy is now known to have a high prevalence in the asymptomatic diabetic patient, prevention at the earliest stage of development by existing molecules would be appropriate in order to prevent the progression of heart failure. In this study, we investigated the protective role of multiple antioxidants (MA), on cardiac dysfunction and cardiac cell apoptosis in streptozotocin (STZ)-induced diabetic rat. Diabetic cardiomyopathy in STZ-treated animals was characterized by declined systolic, diastolic myocardial performance, oxidative stress and apoptosis in cardiac cells. Diabetic rats on supplementation with MA showed decreased oxidative stress evaluated by the content of reduced levels of lipid per-oxidation and decreased activity of catalase with down-regulation of heme-oxygenase-1 mRNA. Supplementation with MA also resulted in a normalized lipid profile and decreased levels of pro-inflammatory transcription factor NF-kappaB as well as cytokines such as TNF-alpha, IFN-gamma, TGF-beta, and IL-10. MA was found to decrease the expression of ROS-generating enzymes like xanthine oxidase, monoamine oxidase-A along with 5-Lipoxygenase mRNA and/or protein expression. Further, left ventricular function, measured by a microtip pressure transducer, was re-established as evidenced by increase in +/-dp/dtmax, heart rate, decreased blood pressure, systolic and diastolic pressure as well as decrease in the TUNEL positive cardiac cells with increased Bcl-2/Bax ratio. In addition, MA supplementation decreased cell death and activation of NF-kappaB in cardiac H9c2 cells. Based on our results, we conclude that MA supplementation significantly attenuated cardiac dysfunction in diabetic rats; hence MA supplementation may have important clinical implications in terms of prevention and management of diabetic cardiomyopathy.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
Diabetic Cardiomyopathies treatmentISOIl10 (Rattus norvegicus)7247697; 7247697 RGD 
Diabetic Cardiomyopathies treatmentIDA 7247697 RGD 
Diabetic Cardiomyopathies treatmentISOXdh (Rattus norvegicus)7247697; 7247697associated with Diabetes Mellitus and ExperimentalRGD 
Diabetic Cardiomyopathies treatmentIDA 7247697associated with Diabetes Mellitus and ExperimentalRGD 

Objects Annotated

Genes (Rattus norvegicus)
Il10  (interleukin 10)
Xdh  (xanthine dehydrogenase)

Genes (Mus musculus)
Il10  (interleukin 10)
Xdh  (xanthine dehydrogenase)

Genes (Homo sapiens)
IL10  (interleukin 10)
XDH  (xanthine dehydrogenase)


Additional Information