Abstract:Objective To investigate the expression of C/EBP homology protein (CHOP) in peripheral brain tissue of patients with severe traumatic brain injury (TBI) and its correlation with the injury severity. Methods The study included peripheral brain tissues of 41 TBI patients (TBI group). Another 16 autopsy specimens succumbed to other diseases (except for TBI or other central nervous system diseases) were selected as controls. The control group and TBI group were subdivided into immaturity group (≤18 years), adult group (18-59 years) and elderly group (>59 years). According to Glasgow Coma Scale (GCS) on admission, TBI group was classified as severe TBI group (GCS of 6-8) and particularly-severe TBI group (GCS of 3-5). CHOP expression in peripheral tissues after TBI was compared in between different age, gender and GCS. Nerve cell apoptosis was detected by TUNEL technique and correlation between CHOP level and apoptotic number was analyzed. Results There were no age and gender differences regarding CHOP expression in control group (P<0.05). Compared with control group, expression of CHOP presented notable up-regulation in TBI group (P<0.05). Expression of CHOP presented no gender difference in TBI group (P>0.05), but its expression was lower in the aged than in adult or immaturity (P<0.05) as well as notably higher in particularly-severe TBI group than in severe TBI group (P<0.05). Nerve cell apoptosis in TBI group was far greater in number than that in control group (P<0.05). A positive correlation was observed between CHOP level and apoptotic index (r=0.72,P<0.05). Conclusion Expression level of CHOP after TBI is closely related to the injury severity and nerve cell apoptosis, but the apoptosis pathway induced by CHOP may not be a major factor in secondary brain injury after TBI in the aged patients.
XIONG Xue-hua,SUN Xiao-chuan,DENG Jian-ping et al. Expression of C/EBP homology protein in patients with severe traumatic brain injury[J]. CHINESE JOURNAL OF TRAUMA, 2013, 29(9): 820-823.
[1]Truettner JS, Hu B, Alonso OF, et al. Subcellular stress response after traumatic brain injury. J Neurotrauma, 2007, 24(4):599-612.
[2]Rubovitch V, Shachar A, Werner H, et al. Does IGF-1 administration after a mild traumatic brain injury in mice activate the adaptive arm of ER stress? Neurochem Int, 2011, 58(4): 443-446.
[3]Krajewska M, Xu L, Xu W, et al. Endoplasmic reticulum protein BI-1 modulates unfolded protein response signaling and protects against stroke and traumatic brain injury. Brain Res, 2011, 1370(1):227-237.
[4]Nathoo N, Narotam PK, Agrawal DK, et al. Influence of apoptosis on neurological outcome following traumatic cerebral contusion. J Neurosurg, 2004, 101(2):233-240
[5]Rutland-Brown W, Langlois JA, Thomas KE, et al. Incidence of traumatic brain injury in the United States. J Head Trauma Rehabil, 2006, 21(6):544-548.
[7]Sandhir R, Puri V, Klein RM, et al. Differential expression of cytokines and chemokines during secondary neuron death following brain injury in old and young mice. Neurosci Lett, 2004, 369(1):28-32.
[8]Moor E, Shohami E, Kanevsky E, et al. Impairment of the ability of the injured aged brain in elevating urate and ascorbate. Exp Gerontol, 2006, 41(3):303-311.
[9]Sandhir RN, Berman E. Age-dependent response of CCAAT/enhancer binding proteins following traumatic brain injury in mice. Neurochem Int, 2010, 56(1): 188-193.
[10]He Z, Ostrowski RP, Sun X, et al. CHOP silencing reduces acute brain injury in the rat model of subarachnoid hemorrhage. Stroke, 2012, 43(2): 484-490.