Abstract:【Objective】 To investigate the correlation between serum neuron specific enolase (NSE), Tau protein, S100 protein, matrix metalloproteinase 9 (MMP-9) and brain edema in patients with traumatic brain injury (TBI).【Methods】Clinical data of 96 patients with traumatic brain injury admitted in our hospital from January 2013 to November 2016 were selected and divided into observation group, and the healthy volunteers were recruited as control group in the same period of time as the control group (n = 60), the brain injury patients were evaluated by head CT examination of brain edema volume at the admission, d3 and d7 after admission. ELISA method was used to detect the serum NSE, Tau, S100, MMP-9 protein levels in the patients with traumatic brain injury , and all the healthy controls were tested for the same index.The serum levels of NSE, Tau, S100 and MMP-9 protein were compared between the two groups, and the correlation between the volume of brain edema and serum protein Pearson was analyzed.【Results】The serum NSE, S100 and MMP-9 in the observation group were higher than those in the control group on the day of admission, the difference was statistically significant (mean P<0.05).The serum Tau protein level in the control group was higher than that in the observation group, but the difference was not statistically significant (P>0.05).The serum NSE, Tau, S100, MMP-9 levels in the observation group were significantly positively correlated with the volume of brain edema (through CT exam) on the day of admission (mean P<0.05);The level of serum S100, MMP-9 and the volume of brain edema in admission d3 were significantly positive (P<0.05).There was a significant positive correlation between serum S100, MMP-9 level and the value development of brain edema.【Conclusion】Serum NSE, Tau, S100 and MMP-9 could reflect the severity of brain edema in TBI, and both MMP-9 and S100 may predict the progress of brain edema, which are valuable in evaluation of the brain edema of TBI patients.
[1] Kimbler DE, Shields J, Yanasak N,et al. Activation of P2X7 promotes cerebral edema and neurological injury after traumatic brain injury in mice[J]. PLoS One, 2012, 7(7): e41229. [2] Winkler EA, Minter D, Yue JK, et al. Cerebral edema in traumatic brain injury: pathophysiology and prospective therapeutic targets[J]. Neurosurg Clin Am, 2016,27(4):473-488. [3] Elwatidy S. Bifrontal decompressive craniectomy is a life-saving procedure for patients with nontraumatic refractory brain edema[J]. Br J Neurosurg, 2009,23(1):56-62. [4] Hatting MT, Smith CT, Radhakrishnan RS, et al. Regional differences in cerebral edema after traumatic brain injury identified by impedance analysis[J]. J Surg Res, 2010,159(1):557-564. [5] 汪开华,谭春棋.S-100蛋白和NSE在脑水肿患者脱水治疗中动态变化[J].国际检验医学杂志,2012,33(9):1055-1056. [6] Yamshita s, Hasuo H, Tokutomi T, et al. Edaravone attenuates impairment of synaptic plasticity in granllle cell layer of the dentate gyms fouowing traumatic brain injury[J].Kumme Med, 2011,58 (2):47-58. [7] imi 'c G, Babi 'c Leko M, Wray S, et al. Tau protein hyperphosphorylation and aggregation in alzheimer's disease and other tauopathies, and possible neuroprotective strategies[J]. Biomolecules, 2016,6(1):6. [8] 宋锦宁,李宇.弥漫性轴索损伤后继发性脑损伤与神经保护治疗的研究进展[J].西安交通大学学报(医学版),2014,35(6):717-725. [9] Cartagena CM, Mountney A, Hwang H, et al. Subacute changes in cleavage processing of amyloid precursor protein and Tau following penetrating traumatic brain injury [J]. PLoS One, 2016,11(7):e0158576. [10] Franz G, Beer R, Kampfl A, et al. Amyloid beta 1-42 and tau in cerebrospinal fluid after severe traumatic brain injury[J]. Neurology, 2003,60(9):1457-1461. [11] 于芸,韩如泉.生物标志物在创伤性颅脑损伤中的应用[J].国际麻醉学与复苏杂志,2013,34(2):126-129. [12] 郑克彬,刘艳峰,刘海鹏,等.基质金属蛋白酶家族在颅脑损伤患者中表达水平的变化[J].中华实验外科杂志,2015,32(1):178-179. [13] 李季林,盛罗平,陈仁辉,等.颅脑损伤后血清中MMP-9、S-100B蛋白的表达对颅脑损伤预后及脑水肿的影响[J].中国医师杂志,2016,18(8):1211-1213.