ROLE OF MELATONIN IN EXPRESSION OF MALONDIALDEHYDE ON MICROGLIA CELLS OF RAT INDUCED HEAD INJURY
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Authors:
Khairul Iksan Nasution
Abstract:
“Background: brain injury is condition that harm human life. This study examines the application of melatonin in reducing oxidant status and barriers to the formation of cerebral edema in a rat brain injury model. The main purpose of this study is to prove the role of melatonin on the expression of Malondialdehyde (MDA) and histological injury in a rat head injury model. Methods: This study was a randomized experimental posttest only control group design. This experimental was carried out on male Sprague Dawley strain Rattus novergicus, aged of 10-12 weeks, and weight of 300 g. Rat brain injury model was performed based on Marmarou (1994).1 Histology were observed using hematoxilen-eosin staining and immunohistochemistry, MDA was assessed using antibodies specific to each MDA protein. Observation and calculation of immunohistochemistry studies were also performed. Results: In this study, histological observation area covers an area of bleeding, number of immune-competent cells and the diameter of the arteries. Histology observation results showed that there is a significant reduction in diameter of arterial blood vessels of the brain injury tissue. Immunohisto-chemistry results showed that there is a significant reduction of MDA expression amount microglia cells of brain injury tissue. Conclusion: From this study, it can be concluded that Melatonin is a potent hydrogen peroxide scavenger that reduce the production of MDA.”
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https://jurnal.harianregional.com/bmj/full-21708
Published
2015-08-28
How To Cite
NASUTION, Khairul Iksan. ROLE OF MELATONIN IN EXPRESSION OF MALONDIALDEHYDE ON MICROGLIA CELLS OF RAT INDUCED HEAD INJURY.BALI MEDICAL JOURNAL, [S.l.], v. 4, n. 2, aug. 2015. ISSN 2302-2914. Available at: https://jurnal.harianregional.com/bmj/id-21708. Date accessed: 28 Aug. 2025.
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Issue
Vol 4 No 2 (2015)
Section
Articles
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This work is licensed under a Creative Commons Attribution 4.0 International License
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