Key result
Aqueous and ethanolic extracts of Cynodon dactylon altered cardiac protein expression in diabetic rats, revealing up-regulation of NTF4 and ETFB proteins.
Why the study?
Does Cynodon dactylon extract alter cardiac protein expression in alloxan-induced diabetic rats?
RCT (n=24)
randomly divided
Does Cynodon dactylon extract alter cardiac protein expression in alloxan-induced diabetic rats?
Proteomic analysis identified NTF4 and ETFB as differentially expressed proteins in the cardiac muscle of diabetic rats, suggesting potential targets for preventing diabetic cardiomyopathy.
Answers are grounded in this paper and cite their sources.
No immediate clinical implications in diabetic cardiomyopathy; hypothesis-generating for NTF4/ETFB as targets in rodent models.
BACKGROUND: 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. METHODS: 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). RESULTS: The above experiment revealed two up-regulated proteins in group-II i.e. NTF4 and ETFB. CONCLUSIONS: 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.
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Karthik et al. (2014) conducted an RCT in diabetic cardiomyopathy (n=24). aqueous and ethanolic extracts of Cynodon dactylon vs. untreated diabetic rats and healthy controls was evaluated on differential protein level in cardiac muscle (p=<0.05). Aqueous and ethanolic extracts of Cynodon dactylon altered cardiac protein expression in diabetic rats, revealing up-regulation of NTF4 and ETFB proteins.
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