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

Year 2011, Volume: 28 Issue: 3, 99 - 102, 09.02.2012

Cevat Aktas , Mehmet Kanter Duygu Uzun Zeynep Fidanol

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

Keywords

-

References

• 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.
• 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.
• 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.
• 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.
• 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.
• 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.
• 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.
• Cohen, G.M., 1997. Caspases: the executioners of apoptosis. Biochem. J. 326, 1–16.
• 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.
• 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.
• 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.
• Henderson, Z., 1996. Responses of basal forebrain cholinergic neurons to damage in the adult brain. Prog. Neurobiol. 48, 219–254.
• 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, H., Hellweg, R., 1997. Insights into the role of the cholinergic component of the septohippocampal pathway: what have we learned from experimental lesion studies? Brain Res. Bull. 43, 245–255.
• Hsu, S.M., Raine, L., Fanger, H., 1981. Use of avidin–biotin-peroxidase complex (ABC) in immunperoxidase techniques: a comparison between ABC and unlabeled antibody (PAP) procedures. J. Histochem. Cytochem. 29, 577-580.
• Ikeda, Y., Long, D.M., 1990. The molecular basis of brain injury and brain edema: the role of oxygen free radicals. Neurosurgery. 27, 1-11.
• Kilbourne, M,M., Kuehn, R., Tosun, C., Caridi, J., Keledjian, K., Bochicchio, G., Scalea, T., Gerzanich, V., Simard, J.J., 2009. Novel model of frontal impact closed head injury in the rat. J. Neurotrauma. 26, 2233-2243.
• Kim, D.H., Ko, I.G., Kim, B.K., Kim, T.W., Kim, S.E., Shin, M.S., Kim, C.J., Kim, H., Kim, K.M., Baek, S.S., 2010. Treadmill exercise inhibits traumatic brain injury-induced hippocampal apoptosis. Physiol. Behav. 101, 660-665.
• Lau, A., Arundine, M., Sun, H.S., Jones, M., Tymianski, M., 2006. Inhibition of caspase-mediated apoptosis by peroxynitrite in traumatic brain injury. J. Neurosci. 26, 11540-11553.
• Lu, J., Moochhala, S., Shirhan, M., Teo, A.L., Tan, M.H., Moore, X.L., Wong, M.C., Ling, E.A., 2003. Neuroprotection by aminoguanidine after lateral fluid-percussive brain injury in rats: a combined magnetic resonance imaging, histopathologic and functional study. Neuropharmacol. 44, 253-263.
• Marshall, L.F., 2000. Head injury: recent past, present, and future. Neurosurgery. 47, 546-561.
• McCall, J.M., Braughler, J.M., Hall, E.D., 1987. Lipide peroxidation and the role of oxygen radicals in CNS injury. Acta. Anaesthesiol. Belg. 38, 373-379.
• Nicholson, D.W., 1999. Caspase structure, proteolytic substrates, and function during apoptotic cell death. Cell. Death. Differ. 6, 1028-1042.
• Oppenheim, R.W., 1991. Cell death during development of the nervous system. Annu. Rev. Neurosci. 14, 453–501.
• Oppenheim, R.W., 1996. The concept of uptake and retrograde transport of neurotrophic molecules during development: history and present status. Neurochem. Res. 21, 769–777.
• Ozsuer, H., Gorgulu, A., Kiris, T., Cobanoglu, S., 2005. The effects of memantine on lipid peroxidation following closed-head trauma in rats. Neurosurg. Rev. 28, 143-147.
• Prange, M.T., Meaney, D.F., Margulies, S.S., 2000. Defining brain mechanical properties: effects of region, direction, and species. Stapp. Car. Crash. J. 44, 205–213.
• Shapira, Y., Shohami, E., Sidi, S., Soffer, D., Freeman, S., Cotev, S., 1988. Experimental closed head injury in rats: mechanical, pathophysiologic and neurologic properties. Crit. Care. Med. 16, 258-265.
• Shen, W.H., Zhang, C.Y., Zhang, G.Y., 2003. Antioxidants attenuate reperfusion injury after global brain ischemia through inhibiting nuclear factor-kappa B activity in rats. Acta Pharmacol. Sin. 24, 1125-1130.
• Siesjo, B.K. 1993. Basic mechanisms of traumatic brain damage. Ann. Emerg. Med. 22, 959-969.
• Sochman, J., 2002. N-acetylcysteine in acute cardiology: 10 years later: what do we know and what would we like to know. J. Am. Coll. Cardiol. 39, 1422-1428.
• Stone, J.R., Okonkwo, D.O., Singleton, R.H., Mutlu, L.K., Helm, G.A., Povlishock, J.T., 2002. Caspase-3-mediated cleavage of amyloid precur- sor protein and formation of amyloid beta peptide in traumatic axonal injury. J. Neurotrauma. 19, 601–614.
• Yakovlev, A.G., Knoblach, S.M., Fan, L., Fox, G.B., Goodnight, R., Faden, A.I., 1997. Activation of CPP32-like caspases contributes to neuronal apoptosis and neurological dysfunction after traumatic brain injury. J. Neurosci. 17, 7415-7424.
• Zimmermann, K.C., Bonzon, C., Green, D.R., 2001. The machinery of programmed cell death. Pharmacol. Ther. 92, 57–70.