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Traumatic Brain Injury-Related Emergency Department Visits, Hospitalizations, and Deaths - United States, 2007 and 2013.2007年和2013年美国与创伤性脑损伤相关的急诊科就诊、住院及死亡情况
MMWR Surveill Summ. 2017 Mar 17;66(9):1-16. doi: 10.15585/mmwr.ss6609a1.
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Study of neurometabolic and behavioral alterations in rodent model of mild traumatic brain injury: a pilot study.轻度创伤性脑损伤啮齿动物模型中的神经代谢和行为改变研究:一项初步研究。
NMR Biomed. 2016 Dec;29(12):1748-1758. doi: 10.1002/nbm.3627. Epub 2016 Oct 25.
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Etifoxine improves sensorimotor deficits and reduces glial activation, neuronal degeneration, and neuroinflammation in a rat model of traumatic brain injury.依替福辛可改善创伤性脑损伤大鼠模型的感觉运动功能障碍,并减轻神经胶质细胞激活、神经元变性和神经炎症。
J Neuroinflammation. 2016 Aug 26;13(1):203. doi: 10.1186/s12974-016-0687-3.
4
Protective effects of taurine in traumatic brain injury via mitochondria and cerebral blood flow.牛磺酸通过线粒体和脑血流量对创伤性脑损伤的保护作用。
Amino Acids. 2016 Sep;48(9):2169-77. doi: 10.1007/s00726-016-2244-x. Epub 2016 May 7.
5
Insight into Pre-Clinical Models of Traumatic Brain Injury Using Circulating Brain Damage Biomarkers: Operation Brain Trauma Therapy.利用循环脑损伤生物标志物深入了解创伤性脑损伤的临床前模型:脑创伤治疗行动
J Neurotrauma. 2016 Mar 15;33(6):595-605. doi: 10.1089/neu.2015.4132.
6
Synthesis of Findings, Current Investigations, and Future Directions: Operation Brain Trauma Therapy.研究结果的综合、当前调查及未来方向:脑外伤治疗行动
J Neurotrauma. 2016 Mar 15;33(6):606-14. doi: 10.1089/neu.2015.4133.
7
Characteristics of Traumatic Brain Injury among Accident and Falling Down Cases.
Acta Med Iran. 2015 Oct;53(10):652-5.
8
Probing astrocyte metabolism in vivo: proton magnetic resonance spectroscopy in the injured and aging brain.体内星形胶质细胞代谢研究:损伤及衰老大脑中的质子磁共振波谱分析
Front Aging Neurosci. 2015 Oct 28;7:202. doi: 10.3389/fnagi.2015.00202. eCollection 2015.
9
A behavioral and histological comparison of fluid percussion injury and controlled cortical impact injury to the rat sensorimotor cortex.大鼠感觉运动皮层液体冲击伤与控制性皮质撞击伤的行为学和组织学比较。
Behav Brain Res. 2015 Nov 1;294:254-63. doi: 10.1016/j.bbr.2015.08.007. Epub 2015 Aug 12.
10
Epidemiology of traumatic brain injury.创伤性脑损伤的流行病学
Handb Clin Neurol. 2015;127:3-13. doi: 10.1016/B978-0-444-52892-6.00001-5.

牛磺酸对创伤性脑损伤老年大鼠的神经保护作用评价。

Evaluation of taurine neuroprotection in aged rats with traumatic brain injury.

机构信息

Hoglund Brain Imaging Center, University of Kansas Medical Center, Kansas City, KS, 66160, USA.

Department of Anatomy and Cell Biology, University of Kansas Medical Center, Kansas City, KS, 66160, USA.

出版信息

Brain Imaging Behav. 2019 Apr;13(2):461-471. doi: 10.1007/s11682-018-9865-5.

DOI:10.1007/s11682-018-9865-5
PMID:29656312
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6186512/
Abstract

Despite higher rates of hospitalization and mortality following traumatic brain injury (TBI) in patients over 65 years old, older patients remain underrepresented in drug development studies. Worse outcomes in older individuals compared to younger adults could be attributed to exacerbated injury mechanisms including oxidative stress, inflammation, blood-brain barrier disruption, and bioenergetic dysfunction. Accordingly, pleiotropic treatments are attractive candidates for neuroprotection. Taurine, an endogenous amino acid with antioxidant, anti-inflammatory, anti-apoptotic, osmolytic, and neuromodulator effects, is neuroprotective in adult rats with TBI. However, its effects in the aged brain have not been evaluated. We subjected aged male rats to a unilateral controlled cortical impact injury to the sensorimotor cortex, and randomized them into four treatment groups: saline or 25 mg/kg, 50 mg/kg, or 200 mg/kg i.p. taurine. Treatments were administered 20 min post-injury and daily for 7 days. We assessed sensorimotor function on post-TBI days 1-14 and tissue loss on day 14 using T-weighted magnetic resonance imaging. Experimenters were blinded to the treatment group for the duration of the study. We did not observe neuroprotective effects of taurine on functional impairment or tissue loss in aged rats after TBI. These findings in aged rats are in contrast to previous reports of taurine neuroprotection in younger animals. Advanced age is an important variable for drug development studies in TBI, and further research is required to better understand how aging may influence mechanisms of taurine neuroprotection.

摘要

尽管 65 岁以上的创伤性脑损伤 (TBI) 患者的住院率和死亡率较高,但在药物开发研究中,老年患者的代表性仍然不足。与年轻成年人相比,老年个体的预后较差可能归因于加剧的损伤机制,包括氧化应激、炎症、血脑屏障破坏和生物能量功能障碍。因此,多效治疗是神经保护的有吸引力的候选物。牛磺酸是一种内源性氨基酸,具有抗氧化、抗炎、抗细胞凋亡、渗透调节和神经调节作用,在 TBI 的成年大鼠中具有神经保护作用。然而,其在老年大脑中的作用尚未得到评估。我们使老年雄性大鼠接受单侧皮质感觉运动区的控制性皮质撞击损伤,并将它们随机分为四组治疗:盐水或 25mg/kg、50mg/kg 或 200mg/kg 腹腔内牛磺酸。治疗在损伤后 20 分钟内进行,每天一次,持续 7 天。我们在 TBI 后第 1-14 天评估感觉运动功能,并在第 14 天使用 T 加权磁共振成像评估组织损失。在整个研究过程中,实验者对治疗组保持盲态。我们没有观察到牛磺酸对 TBI 后老年大鼠的功能障碍或组织损失有神经保护作用。这些在老年大鼠中的发现与以前关于牛磺酸在年轻动物中的神经保护作用的报告相反。年龄是 TBI 药物开发研究的一个重要变量,需要进一步研究以更好地了解衰老如何影响牛磺酸神经保护的机制。