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Knoblach, SM., Faden, AI., Interleukin-10 Improves Outcome and Alter Proinflammatory Cytokine Expression After Experimental Traumatic Brain Injury, ExpNeurol, 1998, Sep;153(1):143-51.

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Article

The Effect of Intervention Recombinant IL-10 on Level of TNF-α and GFAP Serum in the Wistar Rats with Traumatic Brain Injury Treatment

1Department of Surgery, Faculty of Medicine, Hasanuddin University, Makassar, Indonesia

2Neuro Surgery Division, Department of Surgery, Faculty of Medicine, Hasanuddin University, Makassar, Indonesia

3Department of Pediatric, Faculty of Medicine, Hasanuddin University, Makassar, Indonesia


American Journal of Medical and Biological Research. 2017, Vol. 5 No. 1, 9-12
DOI: 10.12691/ajmbr-5-1-2
Copyright © 2017 Science and Education Publishing

Cite this paper:
Yusfitaria Alvina, Andi Asadul Islam, Willy Adhimartha, Idham Jaya Ganda, Prihantono Prihantono. The Effect of Intervention Recombinant IL-10 on Level of TNF-α and GFAP Serum in the Wistar Rats with Traumatic Brain Injury Treatment. American Journal of Medical and Biological Research. 2017; 5(1):9-12. doi: 10.12691/ajmbr-5-1-2.

Correspondence to: Prihantono  Prihantono, Department of Surgery, Faculty of Medicine, Hasanuddin University, Makassar, Indonesia. Email: prihantono.md@gmail.com

Abstract

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.

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