Oxidative Stress and Inflammatory Response in Early Stage of Diffuse Axonal Injury in Rats
Affiliation(s)
Department of Neurosurgery, The First Affiliated Hospital, Medical School of Xi’an Jiaotong University, Xi’an, China.
Department of Neurosurgery, The First Affiliated Hospital, Medical School of Xi’an Jiaotong University, Xi’an, China.
ABSTRACT
Objective: To investigate the role of oxidative stress and immunoinflammatory reaction in early stage of diffuse axonal injury (DAI). Methods: 96 adult male SD rats were divided into 2 groups (n = 48 in each): sham group and DAI group. Rat diffuse axonal injury was induced by a rat instant lateral head rotation device, which was developed to let the rat head spin 90 degree at the moment to cause shearing injury. The modified neurological severity score (mNSS), histomorphology, PI staining, GFAP immunofluorescent staining, SOD activity, CAT activity, MDA content and western blotting (IL-6,IL-1, JNK and p-JNK) in parietal cortex were investigated at 6 h, 1 d and 3 d after DAI. Results: The neurological severity scores, GFAP positive cell, PI positive cells, MDA, IL-6, IL-1, JNK and p-JNK were significantly increased and the SOD and CAT activities were decreased after DAI. Conclusion: Oxidative stress and immunoinflammatory reaction played important roles in DAI pathophysiological process in acute phase.
Objective: To investigate the role of oxidative stress and immunoinflammatory reaction in early stage of diffuse axonal injury (DAI). Methods: 96 adult male SD rats were divided into 2 groups (n = 48 in each): sham group and DAI group. Rat diffuse axonal injury was induced by a rat instant lateral head rotation device, which was developed to let the rat head spin 90 degree at the moment to cause shearing injury. The modified neurological severity score (mNSS), histomorphology, PI staining, GFAP immunofluorescent staining, SOD activity, CAT activity, MDA content and western blotting (IL-6,IL-1, JNK and p-JNK) in parietal cortex were investigated at 6 h, 1 d and 3 d after DAI. Results: The neurological severity scores, GFAP positive cell, PI positive cells, MDA, IL-6, IL-1, JNK and p-JNK were significantly increased and the SOD and CAT activities were decreased after DAI. Conclusion: Oxidative stress and immunoinflammatory reaction played important roles in DAI pathophysiological process in acute phase.
Cite this paper
Ma, X. , Song, J. and Zhao, Y. (2015) Oxidative Stress and Inflammatory Response in Early Stage of Diffuse Axonal Injury in Rats. Journal of Biosciences and Medicines, 3, 9-16. doi: 10.4236/jbm.2015.310002.
Ma, X. , Song, J. and Zhao, Y. (2015) Oxidative Stress and Inflammatory Response in Early Stage of Diffuse Axonal Injury in Rats. Journal of Biosciences and Medicines, 3, 9-16. doi: 10.4236/jbm.2015.310002.
References
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http://dx.doi.org/10.1016/S1388-2457(03)00258-X [8] Laird, M.D., Vender, J.R. and Dhandapani, K.M. (2008) Opposing Roles for Reactive Astrocytes Following Traumatic Brain Injury. Neurosignals, 16, 154-164. http://dx.doi.org/10.1159/000111560 [9] Rodriguez-Rodriguez, A., Egea-Guerrero, J.J., Murillo-Cabezas, F. and Carrillo-Vico, A. (2014) Oxidative Stress in Traumatic Brain Injury. Current Medicinal Chemistry, 21, 1201-1211.
http://dx.doi.org/10.2174/0929867321666131217153310 [10] Mustafa, A.G. and Al-Shboul, O.A. (2013) Pathophysiology of Traumatic Brain Injury. Neurosciences, 18, 222-234. [11] National Research Council (1996) Guide for the Care and Use of Laboratory Animals. 7th Edition, National Academy Press, Washington DC. [12] Li, Y., Song, J.N., Liu, X.B., Zhang, M., Sun, P., Li, D., Jin, T. and Wang, J.F. (2013) High Expression of STIM1 in the Early Stage of Diffuse Axonal Injury. Brain Research, 1495, 95-102.
http://dx.doi.org/10.1016/j.brainres.2012.12.005 [13] Chen, J.L. (2001) Therapeutic Benefit of Intravenous Administration of Bone Marrow Stromal Cells after Cerebral Ischemia in Rats. Stroke, 32, 1005-1011. http://dx.doi.org/10.1161/01.STR.32.4.1005 [14] Krave, U., Hojer, S. and Hansson, H.A. (2005) Transient, Powerful Pressures Are Generated in the Brain by a Rotational Acceleration Impulse to the Head. European Journal of Neuroscience, 21, 2876-2882.
http://dx.doi.org/10.1111/j.1460-9568.2005.04115.x [15] Chen, G., Go, L. and Mao, B. (2002) Biomechanical Mechanism of Diffuse Axonal Injury. Journal of Biomedical Engineering, 19, 500-504. [16] Smith, D.H., Hicks, R. and Povlishock, J.T. (2013) Therapy Development for Diffuse Axonal Injury. Journal of Neurotrauma, 30, 307-323. http://dx.doi.org/10.1089/neu.2012.2825 [17] Lin, Y. and Wen, L. (2013) Inflammatory Response Following Diffuse Axonal Injury. International Journal of Medical Sciences, 10, 515-521. http://dx.doi.org/10.7150/ijms.5423 [18] Campbell, S.J., Deacon, R.M., Jiang, Y., Ferrari, C., Pitossi, F.J. and Anthony, D.C. (2007) Overexpression of IL-1beta by Adenoviral-Mediated Gene Transfer in the Rat Brain Causes a Prolonged Hepatic Chemokine Response, Axonal Injury and the Suppression of Spontaneous Behaviour. Neurobiology of Disease, 27, 151-163. http://dx.doi.org/10.1016/j.nbd.2007.04.013 [19] Tilg, H., Trehu, E., Atkins, M.B., Dinarello, C.A. and Mier, J.W. (1994) Interleukin-6 (IL-6) as an Anti-Inflammatory Cytokine: Induction of Circulating IL-1 Receptor Antagonist and Soluble Tumor Necrosis Factor Receptor p55. Blood, 83, 113-118. [20] Scheller, J., Chalaris, A., Schmidt-Arras, D. and Rose-John, S. (2011) The Pro- and Anti-Inflammatory Properties of the Cytokine Interleukin-6. Biochimica et Biophysica Acta, 1813, 878-888.
http://dx.doi.org/10.1016/j.bbamcr.2011.01.034 [21] Wang, L.W., Tu, Y.F., Huang, C.C. and Ho, C.J. (2012) JNK Signaling Is the Shared Pathway Linking Neuroinflammation, Blood-Brain Barrier Disruption, and Oligodendroglial Apoptosis in the White Matter Injury of the Immature Brain. Journal of Neuroinflammation, 9, 175.
http://dx.doi.org/10.1186/1742-2094-9-175
[1] Romodanovsky, P.O. (2013) Certain Aspects of Diffuse Axonal Injury to the Brain in the Case of Head Trauma. Sudebno-meditsinskaya Ekspertiza, 56, 18-20. [2] Gennarelli, T.A., Thibault, L.E. and Graham, D.I. (1998) Diffuse Axonal Injury: An Important Form of Traumatic Brain Damage. Neuroscientist, 4, 202-215. http://dx.doi.org/10.1177/107385849800400316 [3] Smith, D.H., Meaney, D.F. and Shull, W.H. (2003) Diffuse Axonal Injury in Head Trauma. Journal of Head Trauma Rehabilitation, 18, 307-316. http://dx.doi.org/10.1097/00001199-200307000-00003 [4] Xiong, Y., Mahmood, A. and Chopp, M. (2013) Animal Models of Traumatic Brain Injury. Nature Reviews Neuroscience, 14, 128-142. http://dx.doi.org/10.1038/nrn3407 [5] Masel, B.E. and Dewitt, D.S. (2010) Traumatic Brain Injury: A Disease Process, Not an Event. Journal of Neurotrauma, 27, 1529-1540. http://dx.doi.org/10.1089/neu.2010.1358 [6] Song, J.N. and Li, Y. (2014) Research Advances of Secondary Brain Injury Caused by Diffuse Axonal Injury and Its Therapeutic Strategies. Journal of Xi’an Jiaotong University, Medical Sciences, 35, 717-725. [7] Gaetz, M. (2004) The Neurophysiology of Brain Injury. Clinical Neurophysiology, 115, 4-18.
http://dx.doi.org/10.1016/S1388-2457(03)00258-X [8] Laird, M.D., Vender, J.R. and Dhandapani, K.M. (2008) Opposing Roles for Reactive Astrocytes Following Traumatic Brain Injury. Neurosignals, 16, 154-164. http://dx.doi.org/10.1159/000111560 [9] Rodriguez-Rodriguez, A., Egea-Guerrero, J.J., Murillo-Cabezas, F. and Carrillo-Vico, A. (2014) Oxidative Stress in Traumatic Brain Injury. Current Medicinal Chemistry, 21, 1201-1211.
http://dx.doi.org/10.2174/0929867321666131217153310 [10] Mustafa, A.G. and Al-Shboul, O.A. (2013) Pathophysiology of Traumatic Brain Injury. Neurosciences, 18, 222-234. [11] National Research Council (1996) Guide for the Care and Use of Laboratory Animals. 7th Edition, National Academy Press, Washington DC. [12] Li, Y., Song, J.N., Liu, X.B., Zhang, M., Sun, P., Li, D., Jin, T. and Wang, J.F. (2013) High Expression of STIM1 in the Early Stage of Diffuse Axonal Injury. Brain Research, 1495, 95-102.
http://dx.doi.org/10.1016/j.brainres.2012.12.005 [13] Chen, J.L. (2001) Therapeutic Benefit of Intravenous Administration of Bone Marrow Stromal Cells after Cerebral Ischemia in Rats. Stroke, 32, 1005-1011. http://dx.doi.org/10.1161/01.STR.32.4.1005 [14] Krave, U., Hojer, S. and Hansson, H.A. (2005) Transient, Powerful Pressures Are Generated in the Brain by a Rotational Acceleration Impulse to the Head. European Journal of Neuroscience, 21, 2876-2882.
http://dx.doi.org/10.1111/j.1460-9568.2005.04115.x [15] Chen, G., Go, L. and Mao, B. (2002) Biomechanical Mechanism of Diffuse Axonal Injury. Journal of Biomedical Engineering, 19, 500-504. [16] Smith, D.H., Hicks, R. and Povlishock, J.T. (2013) Therapy Development for Diffuse Axonal Injury. Journal of Neurotrauma, 30, 307-323. http://dx.doi.org/10.1089/neu.2012.2825 [17] Lin, Y. and Wen, L. (2013) Inflammatory Response Following Diffuse Axonal Injury. International Journal of Medical Sciences, 10, 515-521. http://dx.doi.org/10.7150/ijms.5423 [18] Campbell, S.J., Deacon, R.M., Jiang, Y., Ferrari, C., Pitossi, F.J. and Anthony, D.C. (2007) Overexpression of IL-1beta by Adenoviral-Mediated Gene Transfer in the Rat Brain Causes a Prolonged Hepatic Chemokine Response, Axonal Injury and the Suppression of Spontaneous Behaviour. Neurobiology of Disease, 27, 151-163. http://dx.doi.org/10.1016/j.nbd.2007.04.013 [19] Tilg, H., Trehu, E., Atkins, M.B., Dinarello, C.A. and Mier, J.W. (1994) Interleukin-6 (IL-6) as an Anti-Inflammatory Cytokine: Induction of Circulating IL-1 Receptor Antagonist and Soluble Tumor Necrosis Factor Receptor p55. Blood, 83, 113-118. [20] Scheller, J., Chalaris, A., Schmidt-Arras, D. and Rose-John, S. (2011) The Pro- and Anti-Inflammatory Properties of the Cytokine Interleukin-6. Biochimica et Biophysica Acta, 1813, 878-888.
http://dx.doi.org/10.1016/j.bbamcr.2011.01.034 [21] Wang, L.W., Tu, Y.F., Huang, C.C. and Ho, C.J. (2012) JNK Signaling Is the Shared Pathway Linking Neuroinflammation, Blood-Brain Barrier Disruption, and Oligodendroglial Apoptosis in the White Matter Injury of the Immature Brain. Journal of Neuroinflammation, 9, 175.
http://dx.doi.org/10.1186/1742-2094-9-175