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Title: Investigation into cellular and molecular mechanisms underlying diabetic cardiomyopathy: role of oxidative and nitrative stress therapeutic potential of multiple antioxidants
Researcher: Santosh Kumar
Guide(s): Sitasawad, Sandhya
Keywords: Biotechnology, Diabetes, Neuropathy, Retinopathy, Cardiomyopathy, Insulin
Upload Date: 2-Sep-2011
University: University of Pune
Completed Date: January, 2009
Abstract: Cardiovascular complications characterized by cardiac dysfunction are a leading cause of morbidity and mortality associated with diabetes. There are ample evidences that excess generation of reactive oxygen species (ROS) and reactive nitrogen species (RNS), largely due to hyperglycemia, causes oxidative and nitrosative stress, which further exacerbates the development and progression of diabetic cardiomyopathy. Overproduction and/or insufficient removal of these free radicals result in cardiac dysfunction, damage to cellular proteins, membrane lipids and nucleic acids. Despite overwhelming evidence on the damaging consequences of oxidative and nitrosative stress and its role in experimental diabetes, large scale clinical trials with classic antioxidants failed to demonstrate any benefit for diabetic patients with cardiovascular complications. As our understanding of the mechanisms of free radical generation evolves, it is becoming clear that rather than merely scavenging reactive radicals, a more comprehensive approach aimed at preventing the generation of these reactive species as well as scavenging may prove more beneficial. High glucose (HG) generates reactive oxygen species (ROS) as a result of glucose auto-oxidation. Since glucose oxidase catalyses the oxidation of D-glucose in vitro, we exposed H9c2 cardiac myoblast cells to high glucose (33 mM) and glucose oxidase (1.6 mU/ml) to generate ROS and/or RNS in vitro, and termed it G/GO. Using this model, we tested the hypothesis that NAC, catalase and GSH may exert a beneficial effect in preventing high-glucose mediated cardiac cell apoptosis. Our invitro studies indicate that NAC, catalase and GSH exerts a protective effect on G/GO-induced apoptosis in H9C2 cardiac muscle cells via inhibition of ROS and RNS generation and mitochondrial death pathways.
Pagination: 148p.
Appears in Departments:National Centre for Cell Science

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01_title.pdfAttached File101.82 kBAdobe PDFView/Open
02_dedication.pdf90.37 kBAdobe PDFView/Open
03_table of contents.pdf178.34 kBAdobe PDFView/Open
04_acknowledgement.pdf93.54 kBAdobe PDFView/Open
05_certificate.pdf143.51 kBAdobe PDFView/Open
06_declaration.pdf131.21 kBAdobe PDFView/Open
07_abbreviations.pdf160.39 kBAdobe PDFView/Open
08_abstract.pdf142.51 kBAdobe PDFView/Open
09_chapter 1.pdf2.03 MBAdobe PDFView/Open
10_chapter 2.pdf145.57 kBAdobe PDFView/Open
11_chapter 3.pdf253.54 kBAdobe PDFView/Open
12_chapter 4.pdf1.98 MBAdobe PDFView/Open
13_chapter 5.pdf460.65 kBAdobe PDFView/Open
14_summary.pdf123.82 kBAdobe PDFView/Open
15_bibliography.pdf260.81 kBAdobe PDFView/Open
16_publications.pdf174.53 kBAdobe PDFView/Open

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