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논문 기본 정보

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학술저널
저자정보
Eric Weiss (Department of Surgery Einstein Healthcare Network USA) Teena Dhir (Department of Surgery Einstein Healthcare Network USA) Abigail Collett (Philadelphia College of Osteopathic Medicine USA) Michal Reola (Department of Surgery Einstein Healthcare Network USA) Mark Kaplan (Department of Surgery Einstein Healthcare Network USA) Corrado Minimo (Department of Surgery Einstein Healthcare Network USA) Laurel Omert (Department of Surgery Einstein Healthcare Network USA) Pak Leung (Sidney Kimmel Medical College Thomas Jefferson University USA)
저널정보
대한응급의학회 Clinical and Experimental Emergency Medicine Clinical and Experimental Emergency Medicine Vol.7 No.2
발행연도
2020.1
수록면
87 - 94 (8page)

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Objective Traumatic brain injury (TBI) is characterized by damage to the blood-brain barrier, inflammation, and edema formation. In this pilot study, we aimed to investigate the effects of a complement inhibitor, C1-esterase inhibitor (C1 INH), on brain edema and inflammation in a rat model of mild TBI. Methods Thirty-six male Sprague Dawley rats were randomly assigned to control, TBI, or TBI plus C1 INH groups. TBI and TBI plus C1 INH rats received an injection of saline or 25 IU/kg C1 INH, respectively, with TBI using a weight drop model. Control rats received saline only. Rats were subsequently euthanized and their brain tissue harvested for analysis. The primary outcome was the extent of edema as assessed by the brain’s water content. Secondary outcomes included enzyme-linked immunosorbent assays to determine levels of pro-inflammatory mediators. Results Tumor necrosis factor-α levels were significantly greater in TBI rats than control rats, indicating that inflammation was generated by the weight drop impact. Brain water content following TBI was significantly different between TBI rats treated with C1-INH (78.7%±0.12), untreated TBI rats (79.3%±0.12), and control rats (78.6%±0.15, P=0.001). There was a significant decrease in C3a and interleukin 2 levels among C1 INH–treated rats compared with untreated TBI rats, but no change in levels of tumor necrosis factor-α and S100β. Conclusion C1-INH inhibited the complement pathway, suggesting that C1-INH may have a therapeutic benefit in TBI. Further studies are needed to investigate the effect of C1-INH on clinical outcomes.
#Brain injuries #traumatic #Complement system proteins #Edema #Inflammation #Cytokines

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참고문헌 (30)

참고문헌 신청
Gardner AJ / 2016 / Neuroepidemiology of traumatic brain injury / Handb Clin Neurol 138:207~223 google schola Taylor CA / 2017 / Traumatic brain injury-related emergency department visits, hospitalizations, and deaths: United States, 2007 and 2013 / MMWR Surveill Summ 66:1~16 google schola Gyoneva S / 2015 / Inflammatory reaction after traumatic brain injury : therapeutic potential of targeting cell-cell communication by chemokines / Trends Pharmacol Sci 36:471~480 google schola Hammad A / 2018 / The role of the complement system in traumatic brain injury : a review / J Neuroinflammation 15:24 google schola Kochanek PM / 2013 / Screening of biochemical and molecular mechanisms of secondary injury and repair in the brain after experimental blast-induced traumatic brain injury in rats / J Neurotrauma 30:920~937 google schola

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