Journals / Journal of Experimental and Clinical Medicine / 2011 / Cilt: 28 - Sayı: 3

Immunohistochemical investigation of caspase-3 in neuronal apoptosis after experimental closed head trauma

Pages
99–102
Publication Date
2012-02-09
DOI
—
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In conclusion, the caspase 3 immunopositivity was increased in degenerating neurons of the frontal cortex tissue following trauma.

📌 3 Key Takeaways

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Objective & Hypothesis:ABSTRACT The aim of this study was to investigate the caspase-3 activity in neuronal apoptosis after experimental closed head trauma model in rats.
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Key Findings & Data:In trauma group, a cranial impact was delivered to the skull from a height of 7 cm at a point just in front of the coronal suture and over the right hemisphere.
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Conclusion & Impact:In conclusion, the caspase 3 immunopositivity was increased in degenerating neurons of the frontal cortex tissue following trauma.
🔬Design:Modeling & Simulation
📍Scope:2011 Verileri
⚙️Variables:Domain Parameters

Abstract

ABSTRACT The aim of this study was to investigate the caspase-3 activity in neuronal apoptosis after experimental closed head trauma model in rats. Twenty adult male rats were randomly divided into two groups: control and trauma groups. In trauma group, a cranial impact was delivered to the skull from a height of 7 cm at a point just in front of the coronal suture and over the right hemisphere. Rats were sacrificed at 12 hours after the onset of injury. Brain tissues were removed for histopathological investigation. In the trauma group, the neurons became extensively dark and degenerated into picnotic nuclei. The number of apoptotic neurons in frontal cortex tissue of trauma group was significantly more than control groups. In conclusion, the caspase 3 immunopositivity was increased in degenerating neurons of the frontal cortex tissue following trauma. The present results indicate that closed head trauma caused degenerative changes and increased caspase 3 immonupositivity in neurons. J. Exp. Clin. Med., 2011; 99-102

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Cite This Article

AKTAS, C., KANTER, M., UZUN, D., FİDANOL, Z. (2012). Immunohistochemical investigation of caspase-3 in neuronal apoptosis after experimental closed head trauma. Journal of Experimental and Clinical Medicine, Cilt: 28 - Sayı: 3, 99–102. https://ajindex.com/articles/679001

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References (13)

  1. Adams, J.H., Doyle, D., Ford, I., Gennarelli, T.A., Graham, D.I., McLellan, D.R., 1989. Diffuse axonal injury in head injury: definition, diagno- sis and grading. Histopathology 15, 49–59.
  2. Adams, J.H., Graham, D.I., Murray, L.S., Scott, G., 1982. Diffuse axonal injury due to nonmissile head injury in humans: an analysis of 45 cases. Ann. Neurol. 12, 557–563.
  3. Cecil, K.M., Hills, E.C., Sandel, M.E., Smith, D.H., McIntosh, T.K., Mannon, L.J., Sinson, G.P., Bagley, L.J., Grossman, R.I., Lenkinski, R.E., 1998. Proton magnetic resonance spectroscopy for detection of axonal injury in the splenium of the corpus callosum of brain-injured patients. J. Neurosurg. 88, 795–801.
  4. Cernak, I., Chapman, S.M., Hamlin, G.P., Vink, R., 2002. Temporal characterisation of pro- and anti-apoptotic mechanisms following diffuse traumatic brain injury in rats. J. Clin. Neurosci. 9, 565–572.
  5. Clark, R.S., Kochanek, P.M., Watkins, S.C., Chen, M., Dixon, C.E., Seidberg, N.A., Melick, J., Loeffert, J.E., Nathaniel, P.D., Jin, K.L, Graham, S.H., 2000. Caspase-3 mediated neuronal death after traumatic brain injury in rats. J. Neurochem. 74, 740-753.
  6. Clarke, P.G., Posada, A., Primi, M.P., Castagne, V., 1998. Neuronal death in the central nervous system during development. Biomed. Pharma- cother. 52, 356–362.
  7. Clausen, F., Lundqvist, H., Ekmark, S., Lewen, A., Ebendal, T., Hillered, L., 2004. Oxygen free radical-dependent activation of extracellular signal-regulated kinase mediates apoptosis-like cell death after traumatic brain injury. J. Neurotrauma. 21, 1168–1182.
  8. Cohen, G.M., 1997. Caspases: the executioners of apoptosis. Biochem. J. 326, 1–16.
  9. Dressler, J., Hanisch, U., Kuhlisch, E., Geiger, K.D., 2007. Neuronal and glial apoptosis in human traumatic brain injury. Int. J. Legal. Med. 121, 365-375.
  10. Gennarelli, T.A., Adams, J.H., Graham, D.I., 1981. Acceleration induced head injury in the monkey. I. The model, its mechanical and physiologi- cal correlates. Acta Neuropathol. Suppl. 7, 23–25.
  11. Gennarelli, T.A., Thibault, L., Adams, J.H., Graham, D.I., Thompson, C.J., Marcincin, R.P., 1982. Diffuse axonal injury and traumatic coma in the primate. Ann. Neurol. 12, 564–574.
  12. Henderson, Z., 1996. Responses of basal forebrain cholinergic neurons to damage in the adult brain. Prog. Neurobiol. 48, 219–254.
  13. Hicdonmez, T., Kanter, M., Tiryaki, M., Parsak, T., Cobanoglu, S., 2006. Neuroprotective effects of n-acetylcysteine on experimental closed head trauma in rats. Neurochem. Res. 31, 473–481. Hörtnagl