by Yusfitaria Alvina, Andi Asadul Islam, Willy Adhimartha, Idham Jaya Ganda and Prihantono Prihantono
Original Research
Traumatic brain injury (TBI) can trigger an inflammation and activation the mediator substances. TNF-α is a major cytokine that has adverse effects in high level. Glial Fibrillary Acidic Protein (GFAP) in brain cells increases in TBI thus can be an accurate biomarker for brain damage. The purposes of this study are to know the intervention effect of IL-10 as an anti-inflammatory to inflammatory processes (pro anti-inflammatory balance) in TBI. This is an experimental laboratory study with a post-test control group design consisting of four treatment groups and one control group. Measurement of Tumor Necrosis Factor α (TNF-α) and GFAP using Enzyme-Linked Immunoabsorbent Assay (ELISA) methods. The result of this study shows Groups with provoked brain injury had significantly higher levels of serum TNF-α (p <0.05) than the control group. Group provoked a brain injury and given recombinant IL-10 did not have increased levels of TNF-α in serum after 1 hour, differ significantly with no intervention of IL-10. The levels of GFAP have no significant difference 1 hour after TBI, and these levels increase at 24 hours. The conclusion is Intervention by IL-10 could decrease the levels of TNF-α serum immediately after TBI in the Wistar rats and the levels of GFAP 24 hours after TBI are increasing persistently although given by intervention of IL-10 or not.
American Journal of Medical and Biological Research. 2017, 5(1), 9-12. DOI: 10.12691/ajmbr-5-1-2
Pub. Date: July 06, 2017
10865 Views3659 Downloads1 Likes
by Francis Gregory Samonte
Original Research
The study of epigenetic has brought about a deeper understanding of developmental programming through a complex network of modifications involving the DNA. While the DNA sequence remains conservative throughout, the mechanism of epigenetic modification involves changes through histone modification, DNA methylation, and chromatin remodeling. The overall dynamic effect of epigenetic modification allows the gene expression to be altered leading to a diverse phenotypical expression; a functional change in the genome without affecting the DNA. The emergence of nutritional neuroepigenetic serves to bring into focus the impact of nutrition as an environmental agent in regulating gene expression patterns leading to phenotypical expression with profound neurological and cognitive implication in later life. This link is supported by evidence from animal models suggesting that epigenetic marks, which are formed following DNA methylation or histone modification, can induce changes leading to developmental diseases or persist into adulthood. The difficulty in understanding the intrinsic biomolecular correlation between 1) epigenetic modification, 2) nutritional imbalance, and 3) cognitive impairment in an animal based model provides a compelling question regarding the developmental origins of cognitive related diseases. There have been few animal model studies involving the molecular basis of neuroepigenetic dysfunction in the relation to overnutrition or under nutrition. The main criteria in this review will focus on the few animal based studies in nutrition based epigenetic reprogramming and its role in neuroepigenetic dysregulation and cognitive impairment.
American Journal of Medical and Biological Research. 2017, 5(1), 1-8. DOI: 10.12691/ajmbr-5-1-1
Pub. Date: May 25, 2017
10345 Views3249 Downloads