A proteomics approach to identify the differential protein level in cardiac muscle of diabetic rat.

Dhanaraj Karthik; Ravichandran Vijayakumar; Kalailingam Pazhanichamy; Sivanesan Ravikumar

doi:10.18388/abp.2014_1898

Dhanaraj Karthik Department of Biotechnology, PRIST University, Vallam, Thanjavur, Tamilnadu, India.;
Ravichandran Vijayakumar Aquatic Animal Health and Environment Division, Central Institute of Brackishwater Aquaculture-CIBA (ICAR), Chennai, Tamilnadu, India.;
Kalailingam Pazhanichamy Department of Biotechnology, Periyar Maniammai University, Vallam, Thanjavur, Tamilnadu, India.;
Sivanesan Ravikumar Department of Biotechnology, PRIST University, Vallam, Thanjavur, Tamilnadu, India.;

DOI: https://doi.org/10.18388/abp.2014_1898

Abstract

Cardiovascular proteomics investigation reveals the characterization and elucidation of the novel therapeutic targets and strategies to prevent the development of heart failure associated diabetic complication by using 2DE and MS. The experimental animals were made diabetic with a single intraperitoneal injection of alloxan (150 mg/kg of bw). Albino rats were randomly divided into four individual groups: Group-I control (n=6), group-II alloxan-induced diabetic rats, untreated (n=6), group-III (n=6) and group-IV (n=6) alloxan-induced diabetic rats were treated with aqueous and ethanolic extracts of Cynodon dactylon for 15 days, respectively. Animals were euthanized to collect the heart tissues and blood samples. 2DE sample preparation, gel running and staining (n=6: each groups) were performed at the same time to avoid variation. The result of six gel images from each group were analyzed and evaluated as one match set with 2D software (P<0.05). The above experiment revealed two up-regulated proteins in group-II i.e. NTF4 and ETFB. NTF4 is a neuro-protective agent for neuro-degenerative diseases. It will prevent diabetic secondary complications, such as diabetic polyneuropathy and cardiomyopathy. ETFB is active in the mitochondria, the energy-producing centres in cells. It is clear from the experiment that because of up-regulation of ETFB more energy is availabile and the electron transfer for heart during diabetes is possible, what leads to reduce the oxidative stress and free-radical formation. The up-regulated proteins reduced CVD that occurred just before overt hyperglycaemia due to administration of C. dactylon. This approach established the preliminary reference map for decoding cellular mechanisms linked between pathogenesis CVD and diabetes.