创伤性脑损伤模型研究进展
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摘要
创伤性脑损伤(traumatic brain injury,TBI)不仅发病率和死亡率较高,而且也会导致其幸存者的认知活动和感觉运动功能产生不同程度的障碍。建立合理的TBI模型有助于理解TBI病理生理机制并探索其治疗方案。许多创伤性脑损伤动物模型(属体内模型,in vivo TBI model)已被用来复制人类各种创伤性脑损伤,遗憾的是,在动物实验中具有神经保护作用的治疗方案在临床研究中大多无效。由于体外培养的细胞未掺杂体内复杂的影响因素,各种创伤性脑损伤体外模型(in vitro TBI model)被逐步建立起来。根据致伤方式的不同,可将常用的体内动物模型和体外细胞模型分为机械作用力损伤模型、压力损伤模型、爆炸伤模型、反复性轻度损伤模型。对上述常用TBI模型的特点进行了综述和比较分析,以期为寻找在临床上具有神经保护效果的策略提供帮助。
Traumatic brain injury( TBI) not only has higher morbidity and mortality,but also leads to varying degrees of impairment in cognitive activities and sensorimotor functions of its survivors. Establishing a reasonable TBI model helps to understand the pathophysiology of TBI and explore its treatment strategies. Many animal models of traumatic brain injury( belong to in vivo TBI models) have already been used to replicate various traumatic brain injuries in human. Unfortunately,most of the therapeutic regimens with neuroprotective effects in animal experiments proved to be ineffective in clinical studies. Since cells cultured in vitro are not adulterated with complex factors which exit in vivo,in vitro models of various traumatic brain injuries have been set up progressively. According to different types of injury,the common-used in vivo animal models and in vitro cell models are divided into physical injury model,pressure injury model,blast-induced injury model and repeated mild injury model. The characteristics of the above common-used TBI models were summarized and comparatively analyzed in order to help for the search of clinical strategies with neuroprotective effects.
Traumatic brain injury( TBI) not only has higher morbidity and mortality,but also leads to varying degrees of impairment in cognitive activities and sensorimotor functions of its survivors. Establishing a reasonable TBI model helps to understand the pathophysiology of TBI and explore its treatment strategies. Many animal models of traumatic brain injury( belong to in vivo TBI models) have already been used to replicate various traumatic brain injuries in human. Unfortunately,most of the therapeutic regimens with neuroprotective effects in animal experiments proved to be ineffective in clinical studies. Since cells cultured in vitro are not adulterated with complex factors which exit in vivo,in vitro models of various traumatic brain injuries have been set up progressively. According to different types of injury,the common-used in vivo animal models and in vitro cell models are divided into physical injury model,pressure injury model,blast-induced injury model and repeated mild injury model. The characteristics of the above common-used TBI models were summarized and comparatively analyzed in order to help for the search of clinical strategies with neuroprotective effects.
引文
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[3] Taylor C A,Bell J M,Breiding M J,et al.. Traumatic brain injury-related emergency department visits, hospitalizations,and deaths-United States, 2007 and 2013[J]. MMWR Surveill. Summ.,2017,66(9):1-16.
[4] Majdan M,Plancikova D,Brazinova A,et al.. Epidemiology of traumatic brain injuries in Europe:A cross-sectional analysis[J]. Lancet Public Health,2016,1(2):e76-e83.
[5] Cheng P,Yin P,Ning P,et al.. Trends in traumatic brain injury mortality in China,2006-2013:A population-based longitudinal study[J]. PLoS Med.,2017,14(7):e1002332.
[6] Scott G,Ramlackhansingh A F,Edison P,et al.. Amyloid pathology and axonal injury after brain trauma[J]. Neurology,2016,86(9):821-828.
[7] Jafari S,Etminan M,Aminzadeh F,et al.. Head injury and risk of Parkinson disease:A systematic review and metaanalysis[J]. Movement Disord.,2013,28(9):1222-1229.
[8] Webster K M,Sun M,Crack P,et al.. Inflammation in epileptogenesis after traumatic brain injury[J]. J. Neuroinflamm.,2017,14:10.
[9] De Kosky S T,Blennow K,Ikonomovic M D,et al.. Acute and chronic traumatic encephalopathies:Pathogenesis and biomarkers[J]. Nat. Rev. Neurol.,2013,9(4):192-200.
[10] Hou J,Nelson R,Wilkie Z,et al.. Mild and mild-to-moderate traumatic brain injury-induced significant progressive and enduring multiple comorbidities[J]. J. Neurotraum.,2017,34(16):2456-2466.
[11] Xiong Y,Mahmood A,Chopp M. Animal models of traumatic brain injury[J]. Nat. Rev. Neurosci.,2013,14(2):128
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[13] Maramarou A,Foda M A,van den Brink W. A new model of diffuse brain injury in rats[J]. J. Neurosurg.,1994,80(2):301-313.
[14] Feeney D M,Boyeson M G,Linn R T,et al.. Responses to cortical injury:I. Methodology and local effects of contusions in the rat[J]. Brain Res.,1981,211(1):67-77.
[15] Pang A L,Xiong L L,Xia Q J,et al.. Neural stem cell transplantation is associated with inhibition of apoptosis,Bcl-xL upregulation,and recovery of neurological function in a rat model of traumatic brain injury[J]. Cell Transplant.,2017,26(7):1262-1275.
[16] Chen X,Wu S,Chen C,et al.. Omega-3 polyunsaturated fatty acid supplementation attenuates microglial-induced inflammation by inhibiting the HMGB1/TLR4/NF-κB pathway following experimental traumatic brain injury[J]. J. Neuroinflamm.,2017,14:143.
[17] Jia J,Chen F,Wu Y. Recombinant PEP-1-SOD1 improves functional recovery after neural stem cell transplantation in rats with traumatic brain injury[J]. Exp. Ther. Med.,2018,15(3):2929-2935.
[18] He H,Liu W,Zhou Y,et al.. Sevoflurane post-conditioning attenuates traumatic brain injury-induced neuronal apoptosis by promoting autophagy via the PI3K/AKT signaling pathway[J].Drug Des. Dev. Ther.,2018,12:629-638.
[19] Lighthall J W. Controlled cortical impact:A new experimental brain injury model[J]. J. Neurotraum.,1988,5(1):1-15.
[20] Wang W,Zhang H,Lee D H,et al.. Using functional and molecular MRI techniques to detect neuroinflammation and neuroprotection after traumatic brain injury[J]. Brain Behav. Immun.,2017,64:344-353.
[21] Cheng S X,Xu Z W,Yi T L,et al.. i TRAQ-based quantitative proteomics reveals the new evidence base for traumatic brain injury treated with targeted temperature management[J]. Neurotherapeutics,2018,15(1):216-232.
[22] Wang L,Zhao C,Wu S,et al.. Hydrogen gas treatment improves the neurological outcome after traumatic brain injury via increasing miR-21 expression[J]. Shock,2018,50(3):308-315.
[23] Leary J B,Bondi C O,La Porte M J,et al.. The therapeutic efficacy of environmental enrichment and methylphenidate alone and in combination after controlled cortical impact injury[J]. J.Neurotraum.,2017,34(2):444-450.
[24] Faden A I,Movsesyan V A,Knoblach S M,et al.. Neuroprotective effects of novel small peptides in vitro and after brain injury[J]. Neuropharmacology,2005,49(3):410-424.
[25]黄卫东,费舟,章翔,等.体外培养大鼠脑皮层神经元机械性损伤模型的建立[J].第四军医大学学报,2004,25(4):307-309.
[26] Liu W,Chen Y,Meng J,et al.. Ablation of caspase-1 protects against TBI-induced pyroptosis in vitro and in vivo[J]. J. Neuroinflamm.,2018,15:48.
[27] Saykally J N,Hatic H,Keeley K L,et al.. Withania somnifera extract protects model neurons from in vitro traumatic injury[J]. Cell Transplant.,2017,26(7):1193-1201.
[28] Cater H L,Sundstrom L E,Morrison III B. Temporal development of hippocampal cell death is dependent on tissue strain but not strain rate[J]. J. Biomech.,2006,39(15):2810-2818.
[29] Salvador E,Burek M,F9rster C Y. Stretch and/or oxygen glucose deprivation(OGD)in an in vitro traumatic brain injury(TBI)model induces calcium alteration and inflammatory cascade[J]. Front. Cell. Neurosci.,2015,9:323.
[30] Yap Y C,King A E,Guijt R M,et al.. Mild and repetitive very mild axonal stretch injury triggers cytoskeletal mislocalization and growth cone collapse[J]. PLoS ONE,2017,12(5):e0176997.
[31] Shrirao A B,Kung F H,Omelchenko A,et al.. Microfluidic platforms for the study of neuronal injury in vitro[J].Biotechnol. Bioeng.,2018,115(4):815-830.
[32] Dixon C E,Lyeth B G,Povlishock J T,et al.. A fluid percussion model of experimental brain injury in the rat[J]. J. Neorosurg.,1987,67(1):110-119.
[33] Morales D M,Marklund N,Lebold D,et al.. Experimental models of traumatic brain injury:Do we really need to build a better mousetrap?[J]. Neuroscience,2005,136(4):971-989.
[34] Alder J,Fujioka W,Lifshitz J,et al.. Lateral fluid percussion:Model of traumatic brain injury in mice[J]. J. Vis. Exp.,2011(54):e3063.
[35] Liu Y R,Cardamone L,Hogan R E,et al.. Progressive metabolic and structural cerebral perturbations after traumatic brain injury:An in vivo imaging study in the rat[J]. J. Nucl. Med.,2010,51(11):1788-1795.
[36] Evans L P,Newell E A,Mahajan M A,et al.. Acute vitreoretinal trauma and inflammation after traumatic brain injury in mice[J]. Ann. Clin. Trans. Neurol.,2018,5(3):240-251.
[37] Fehily B,Fitzgerald M. Repeated mild traumatic brain injury:Potential mechanisms of damage[J]. Cell Transplant.,2017,26(7):1131-1155.
[38] Kabadi S V,Hilton G D,Stoica B A,et al.. Fluid-percussioninduced traumatic brain injury model in rats[J]. Nat. Protoc.,2010,5(9):1552.
[39] Davis A R,Shear D A,Chen Z,et al.. A comparison of two cognitive test paradigms in a penetrating brain injury model[J].J. Neurosci. Meth.,2010,189(1):84-87.
[40] Shear D A,Lu X C M,Pedersen R,et al.. Severity profile of penetrating ballistic-like brain injury on neurofunctional outcome,blood-brain barrier permeability,and brain edema formation[J]. J. Neurotraum.,2011,28(10):2185-2195.
[41]陈翰博.下调水通道蛋白-4在脑水肿时可能产生双刃剑作用的研究[D].昆明:昆明医科大学,博士学位论文,2015.
[42] Popova D,Karlsson J, Jacobsson S O P. Comparison of neurons derived from mouse P19,rat PC12 and human SHSY5Y cells in the assessment of chemical-and toxin-induced neurotoxicity[J]. BMC Pharmacol. Toxicol.,2017,18:42.
[43]张永和,赵宁,易声禹,等.气压致离体中枢神经细胞损伤模型[J].第四军医大学学报,2002,23(5):423-425.
[44] Smith M E, Eskandari R. A novel technology to model pressure-induced cellular injuries in the brain[J]. J. Neurosci.Meth.,2018,293:247-253.
[45] Zhou B,Yu P,Lin M Y,et al.. Facilitation of axon regeneration by enhancing mitochondrial transport and rescuing energy deficits[J]. J. Cell Biol.,2016,214(1):103-119.
[46] Kovacs S K,Leonessa F,Ling G S F. Blast TBI models,neuropathology,and implications for seizure risk[J]. Front. Neurol.,2014,5:47.
[47] Risling M,Plantman S,Angeria M,et al.. Mechanisms of blast induced brain injuries,experimental studies in rats[J].Neuroimage,2011,54:S89-S97.
[48]楚燕飞,李兵仓,陈菁,等.大鼠爆炸性脑创伤模型建立[J].第三军医大学学报,2006,28(6):606-607.
[49] Rodriguez U A,Zeng Y,Deyo D,et al.. Effects of mild blast traumatic brain injury on cerebral vascular,histopathological,and behavioral outcomes in rats[J]. J. Neurotraum.,2018,35(2):375-392.
[50]李彦腾,程岗,刘邦鑫,等.几种颅脑爆震伤动物模型建立方法的比较[J].中华神经外科疾病研究杂志,2017,16(1):87-89.
[51] Wang Z,Sun L,Yang Z,et al.. Development of serial bioshock tubes and their application[J]. Chin. Med. J.,1998,111(2):109-113.
[52] Campos-Pires R,Dickinson R. Modelling Blast Brain Injury[A]. In:Bull A M J,Clasper J,Mahoney P F. Blast injury science and engineering:A guide for clinicians and researchers[M]. New York:Springer,2016,173-182.
[53] Campos-Pires R, Koziakova M, Yonis A, et al.. Xenon protects against blast-induced traumatic brain injury in an in vitro model[J]. J. Neurotraum.,2018,35(8):1037-1044.
[54] Lithgow K,Chin A,Debert C T,et al.. Utility of serum IGF-1for diagnosis of growth hormone deficiency following traumatic brain injury and sport-related concussion[J]. BMC Endocr.Disord.,2018,18:20.
[55] Yu F,Shukla D K,Armstrong R C,et al.. Repetitive model of mild traumatic brain injury produces cortical abnormalities detectable by magnetic resonance diffusion imaging,histopathology,and behavior[J]. J. Neurotraum.,2017,34(7):1364-1381.
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