Journals / Turkish Neurosurgery / 2016 / Cilt: 26 - Sayı: 3

Changes of MDA and SOD in Brain Tissue after Secondary Brain Injury with Seawater Immersion in Rats

Pages
384–388
DOI
—
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⚡ TL;DR(Too Long; Didn't Read)

CONCLUSION: The SBI with seawater immersion is faster and more serious than the simple SBI

📌 3 Key Takeaways

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Objective & Hypothesis:AIM: To investigate the variation and significance of malondialdehyde (MDA) and superoxide dismutase (SOD) in brain tissue after secondary brain injury (SBI) with seawater immersion in rats.
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Key Findings & Data:MATERIAL and METHODS: We randomly divided 163 male Sprague Dawley rats into 4 groups, as normal (Group A), SBI (Group B), SBI with physiological saline immersion (Group C) and SBI with seawater immersion (Group D) groups.
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Conclusion & Impact:CONCLUSION: The SBI with seawater immersion is faster and more serious than the simple SBI
🔬Design:Modeling & Simulation
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters

Özet

AIM: To investigate the variation and significance of malondialdehyde (MDA) and superoxide dismutase (SOD) in brain tissue after secondary brain injury (SBI) with seawater immersion in rats. MATERIAL and METHODS: We randomly divided 163 male Sprague Dawley rats into 4 groups, as normal (Group A), SBI (Group B), SBI with physiological saline immersion (Group C) and SBI with seawater immersion (Group D) groups. The animal model of ischemic SBI with seawater immersion was established based on the Marmarou's model of diffuse brain injury. The water content, and the MDA and SOD contents of brain tissue were detected at 1, 3, 6, 12, 24 and 48 hours after the injury. RESULTS: Compared to group A, there were significant changes of various indicators in group D after injury at 1 hour after injury (P < 0.05). The water content and MDA contents in brain tissue were persistently elevated and significantly higher than that in groups B and C at each time phase (P < 0.05). The SOD content showed a persistent decline and was significantly lower than that in groups B and C at each time phase (P < 0.05). The SOD content was negatively correlated with the MDA content with a correlation coefficient of -0.992 (P < 0.01). CONCLUSION: The SBI with seawater immersion is faster and more serious than the simple SBI

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Cite This Article

WEI, L. F., ZHANG, H., WANG, S., JING, J., ZHENG, Z., GAO, J., LIU, Z., TIAN, J. (2016). Changes of MDA and SOD in Brain Tissue after Secondary Brain Injury with Seawater Immersion in Rats. Turkish Neurosurgery, Cilt: 26 - Sayı: 3, 384–388. https://ajindex.com/articles/404676

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References (1)

  1. Al-Samsam RH, Alessandri B, Bullock R: Extracellular Nacetylaspartate as a biochemical marker of the severity of neuronal damage following experimental acute traumatic brain injury. J Neurotrauma 17(1): 31-39, 2002 2. Aoyama N, Lee SM, Moro N, Hovda DA, Sutton RL: Duration of ATP reduction affects extent of CA1 cell death in rat models of fluid percussion injury combined with secondary ischemia. Brain Res 1230: 310-319, 2008 3. Bartfai T, Sanchez-Alavez M, Andell-Jonsson S, Schultzberq M, Vezzani A, Danielsson E, Conti B: Interleukin-1 system in CNS stress: Seizures, fever, and neurotrauma. Ann N Y Acad Sci 1113: 173-l77, 2007 4. Campbell SJ, Jiang Y, Davis AE, Farrands R, Holbrook J, Leppert D, Anthony DC: Immunomodulatory effects of etanercept in a model of brain injury act through attenuation of the acute-phase response. J Neurochem 103(6):2245-2255, 2007 5. Chesnut RM: Secondary brain insults after head injury: Clinical perspectives. New Horiz 3(3): 366-375, 1995 6. Chesnut RM, Marshll LF, Klauber MR: The role of secondary brain injury in determining outcome from severe head injury. J Trauma 34: 216-222, 1993 7. Chi JH, Knudson MM, Vassar MJ, McCarthy MC, Shapiro MB, Mallet S, Holcroft JJ, Moncrief H, Noble J, Wisner D, Kaups KL, Bennick LD, Manley GT: Prehospital hypoxia affects outcome in patients with traumatic brain injury: A prospective multicenter study. J Trauma 61(5):1134-1141, 2006 8. Dearden NM: Mechanisms and prevention of secondary brain damage during intensive care. Clin Neuropathol 17(4):221- 228, 1998 9. Eriskat J, Stoffel M, Plesnila N, Rinecher M, Baethmann A: Interstitial lactate in the peritraumatic penumbra of rat brain. Acta Neurochir Suppl 76:353-355, 2000 10. Gregorakos L, Markou N, Psalida V, Kanakaki M, Alexopoulou A, Sotiriou E, Damianos A, Myrianthefs P: Near-drowning: Clinical course of lung injury in adults. Lung 187(2):93-97, 2009 11. Haddad VJ, Lupi O, Lonza JP, Tyring SK: Tropical dermatology: Marine and aquatic dermatology. J Am Acad Dermatol 61(5): 733-750, 2009 12. Kamm K, Vanderkolk W, Lawrence C, Jonker M, Davis AT: The effect of traumatic brain injury upon the concentration and expression of interleukin-1 beta and interleukin-10 in the rat. J Trauma 60(1):152-157, 2006 13. Kimelberg HK, Mongin AA: Swelling-activated release of excitatory amino acids in the brain: Relevance for pathophysiology. Contrib Nephrol 123: 240-257, 1998 14. Marmarou A, Foda MA, van den Brink W, Campbell J, Kita H, Demetriadou K: A new mo