颅脑损伤的炎症反应
The Inflammatory Response to Craniocerebral Injury
DOI: 10.12677/ACM.2022.124508, PDF, 下载: 255  浏览: 364 
作者: 王焕茹:青海大学研究生院,青海 西宁;马四清*:青海省人民医院重症医学科,青海 西宁
关键词: 颅脑损伤继发性脑损伤炎症反应炎症因子Craniocerebral Injury Secondary Brain Injury Inflammatory Response Inflammatory Factors
摘要: 颅脑损伤是一个难以预料、有多种因素参加的疾病发展过程,其中对脑组织的损伤包括原发性和继发性的损伤。原发性的颅脑损伤包括外力对颅内结构的物理性破坏,是对脑实质和脑血管的直接性损伤,如血肿、挫伤等,其损伤程度及部位无法被临床医生控制及预料病情。但其导致的相关生化途径的激活及作用细胞可被控制及预防病情发展。继发性颅脑损伤可进一步使脑损伤加重,主要是通过兴奋性神经递质活性增强、炎症细胞因子释放和活性氧(ROS)的产生导致的。因此控制炎症反应对脑损伤的病情控制及预后有重要意义,希望能够更好地了解脑损伤的炎症反应的进展,增加更有效的脑损伤治疗方法。
Abstract: Craniocerebral injury is an unpredictable and multifactorial process of disease development, in which brain tissue damage includes primary and secondary damage. Primary craniocerebral injury includes physical destruction of intracranial structure by external forces, and is direct injury to brain parenchyma and cerebrovascular, such as hematoma and contusion. The degree and location of injury cannot be controlled and predicted by clinicians. However, the activation of related biochemical pathways and the cells acting on them can be controlled and prevented from developing the disease. Secondary brain injury can further aggravate brain injury, mainly through increased excitatory neurotransmitter activity, release of inflammatory cytokines and production of reactive oxygen species (ROS). Therefore, the control of inflammatory response is of great significance for the disease control and prognosis of brain injury. It is hoped that we can better understand the progress of inflammatory response of brain injury and increase more effective treatment methods for brain injury.
文章引用:王焕茹, 马四清. 颅脑损伤的炎症反应[J]. 临床医学进展, 2022, 12(4): 3500-3505. https://doi.org/10.12677/ACM.2022.124508

参考文献

[1] Yang, Y., Boza-Serrano, A., Dunning, C.J.R., et al. (2018) Inflammation Leads to Distinct Populations of Extracellular Vesicles from Microglia. Journal of Neuroinflammation, 15, Article No. 168.
https://doi.org/10.1186/s12974-018-1204-7
[2] Akamatsu, Y. and Hanafy, K.A. (2020) Cell Death and Recovery in Traumatic Brain Injury. Neurotherapeutics, 17, 446-456.
https://doi.org/10.1007/s13311-020-00840-7
[3] Morganti-Kossmann, M.C., Rancan, M., Stahel, P.F., et al. (2002) Inflammatory Response in Acute Traumatic Brain Injury: A Double-Edged Sword. Current Opinion in Critical Care, 8, 101-105.
https://doi.org/10.1097/00075198-200204000-00002
[4] Sande, A. and West, C. (2010) Traumatic Brain Injury: A Review of Pathophysiology and Management. Journal of Veterinary Emergency and Critical Care, 20, 177-190.
https://doi.org/10.1111/j.1476-4431.2010.00527.x
[5] 张鹏, 徐志明, 左安俊, 等. S100β、IL-1β与IL-6联合检测对青壮年颅脑损伤诊断及预后评估的价值[J]. 青岛大学学报(医学版), 2019, 55(4): 461-464+468.
[6] Dempsey, R.J., Başkaya, M.K. and Doğan, A. (2000) Attenuation of Brain Edema, Blood-Brain Barrier Breakdown, and Injury Volume by Ifenprodil, a Polyamine-Site N-Methyl-D-Aspartate Receptor Antagonist, after Experimental Traumatic Brain Injury in Rats. Neurosurgery, 47, 399-406.
[7] Villalba, N., Sonkusare, S.K., Longden, T.A., et al. (2014) Traumatic Brain Injury Disrupts Cerebrovascular Tone through Endothelial Inducible Nitric Oxide Synthase Expression and Nitric Oxide Gain of Function. Journal of the American Heart Association, 3, e001474.
https://doi.org/10.1161/JAHA.114.001474
[8] Webster, K.M., Sun, M., Crack, P., et al. (2017) Inflammation in Epileptogenesis after Traumatic Brain Injury. Journal of Neuroinflammation, 14, Article No. 10.
https://doi.org/10.1186/s12974-016-0786-1
[9] Lozano, D., Gonzales-Portillo, G.S., Acosta, S., et al. (2015) Neuroinflammatory Responses to Traumatic Brain Injury: Etiology, Clinical Consequences, and Therapeutic Opportunities. Neuropsychiatric Disease and Treatment, 11, 97-106.
https://doi.org/10.2147/NDT.S65815
[10] 徐跃峤, 王宁, 胡锦, 等. 重症动脉瘤性蛛网膜下腔出血管理专家共识(2015) [J]. 中国脑血管病杂志, 2015, 12(4): 215-225.
[11] Zhu, H., Wang, Z., Yu, J., et al. (2019) Role and Mechanisms of Cytokines in the Secondary Brain Injury after Intracerebral Hemorrhage. Progress in Neurobiology, 178, Article ID: 101610.
https://doi.org/10.1016/j.pneurobio.2019.03.003
[12] Elkabets, M., Ribeiro, V.S.G, Dinarello, C.A., et al. (2010) IL-1β Regulates a Novel Myeloid-Derived Suppressor Cell Subset that Impairs NK Cell Development and Function. European Journal of Immunology, 40, 3347-3357.
https://doi.org/10.1002/eji.201041037
[13] Norelli, M., Camisa, B., Barbiera, G., et al. (2018) Monocyte-Derived IL-1 and IL-6 Are Differentially Required for Cytokine-Release Syndrome and Neurotoxicity Due to CAR T Cells. Nature Medicine, 24, 739-748.
https://doi.org/10.1038/s41591-018-0036-4
[14] 林重辉. 硬膜外血肿清除术中硬膜下腔注水法的实验研究[D]: [硕士学位论文]. 汕头: 汕头大学, 2008.
[15] Wei, X., Hu, C., Zhang, Y., et al. (2016) Telmisartan Reduced Cerebral Edema by Inhibiting NLRP3 Inflammasome in Mice with Cold Brain Injury. Journal of Huazhong University of Science and Technology [Medical Sciences], 36, 576-583.
https://doi.org/10.1007/s11596-016-1628-1
[16] Hayakata, T., Shiozaki, T., Tasaki, O., et al. (2004) Changes in CSF S100B and Cytokine Concentrations in Early-Phase Severe Traumatic Brain Injury. Shock, 22, 102-107.
https://doi.org/10.1097/01.shk.0000131193.80038.f1
[17] 马志海, 张祎年. 炎症反应在脑出血后继发性脑损伤中作用机制的研究进展[J]. 中国临床神经外科杂志, 2020, 25(2): 124-126.
[18] Frugier, T., Morganti-Kossmann, M.C., O’Reilly, D., et al. (2010) In Situ Detection of Inflammatory Mediators in Post Mortem Human Brain Tissue after Traumatic Injury. Journal of Neurotrauma, 27, 497-507.
https://doi.org/10.1089/neu.2009.1120
[19] 袁州, 张一凡. 脑出血破入脑室患者血清IL-1β, IL-6动态变化及与脑循环动力学指标的关系[J]. 中国实用神经疾病杂志, 2011, 14(5): 5-8.
[20] Gebhard, F., Pfetsch, H., Steinbach, G., et al. (2000) Is Interleukin 6 an Early Marker of Injury Severity Following Major Trauma in Humans? Archives of Surgery, 135, 291-295.
https://doi.org/10.1001/archsurg.135.3.291
[21] 闫雪, 刘晶瑶, 刘红超, 等. IL-33在中枢神经系统疾病中的调控作用[J]. 中国实验诊断学, 2020, 24(9): 1567-1570.
[22] Kempuraj, D., Twait, E.C., Williard, D.E., et al. (2013) The Novel Cytokine Interleukin-33 Activates Acinar Cell Proinflammatory Pathways and Induces Acute Pancreatic Inflammation in Mice. PLoS ONE, 8, e56866.
https://doi.org/10.1371/journal.pone.0056866
[23] Suzukawa, M., Koketsu, R., Iikura, M., et al. (2008) Interleukin-33 Enhances Adhesion, CD11b Expression and Survival in Human Eosinophils. Laboratory Investigation, 88, 1245-1253.
https://doi.org/10.1038/labinvest.2008.82
[24] Zhang, Z.Y., Li, J., Ye, Q., et al. (2019) Usefulness of Serum Interleukin-33 as a Prognostic Marker of Severe Traumatic Brain Injury. Clinica Chimica Acta, 497, 6-12.
https://doi.org/10.1016/j.cca.2019.07.008
[25] 罗立峰, 陈隽, 罗仕达, 等. 脑外伤患者检测血浆IL-11的临床评价[J]. 放射免疫学杂志, 2012, 25(5): 577-579.
[26] 张玉敏, 韩素桂, 刘启为, 周琪, 卢军利. 白细胞介素-11在小鼠脑缺血再灌注损伤中的保护作用及其机制[J]. 免疫学杂志, 2021, 37(2): 134-139.
[27] 万小颖, 李挺, 秦立志, 等. 白细胞介素-10研究进展[J]. 畜牧与兽医, 2013(3): 90-94.
[28] Garcia, J.M., Stillings, S.A., Leclerc, J.L., et al. (2017) Role of Interleukin-10 in Acute Brain Injuries. Frontiers in Neurology, 8, Article No. 244.
https://doi.org/10.3389/fneur.2017.00244
[29] Chang, C.F., Wan, J., Li, Q., et al. (2017) Alternative Activation-Skewed Microglia/Macrophages Promote Hematoma Resolution in Experimental Intracerebral Hemorrhage. Neurobiology of Disease, 103, 54-69.
https://doi.org/10.1016/j.nbd.2017.03.016