INTRODUCTION:Management of traumatic brain injury (TBI) is focused on minimizing or preventing secondary brain injury. Remote ischemic conditioning (RIC) is an established treatment modality that has been shown to improve patient outcomes in different clinical settings by influencing inflammatory insults. In a clinical trial, RIC showed amelioration of SB100 and neuron-specific enolase. The aim of our study was to further elucidate the mechanisms and outcome when applying RIC in a mouse model of traumatic brain injury. METHODS:We subjected 100 male C57BL mice to a closed-skull cortical-controlled impact injury. Two hours after the TBI, the animals were allocated to either the RIC group (n = 50) or the sham group (n = 50). By clamping the exposed femoral artery, we induced RIC by six 4-minute cycles of ischemia and reperfusion. Circulating levels of S100-B, neuron-specific enolase, and glial fibrillary acidic protein were measured at multiple time points. Animals were additionally observed daily for cognition and motor coordination via novel object recognition and rotarod. Brain sections were stained and evaluated for neuronal injury at post-TBI Day 5. RESULTS:The RIC animals had a significantly higher recognition index than did sham at 24, 48, and 72 hours after intervention. Rotarod latency was higher in the RIC animals compared to the sham animals at all-time points, and statistically significant at 120 hours after intervention. The RIC group demonstrated preserved cognitive function and motor coordination compared to the sham. On hematoxylin and eosin and immunohistochemical staining of brain sections, there was less area of neuronal degeneration and astrocytosis, respectively, in the RIC group compared to the sham group. There was no significant difference in systemic neuronal markers between the RIC and sham animals. CONCLUSION:Remote ischemic conditioning 2 hours after injury preserved cognitive functions and motor coordination in a mouse model of TBI. Remote ischemic conditioning can preserve viability of neurons and astrocytes after TBI and has potential as a clinically noninvasive and relatively easy method to improve outcome after TBI. LEVEL OF EVIDENCE:Therapeutic studies, randomized controlled trial, level I.

译文

简介:创伤性脑损伤(TBI)的管理重点在于最大程度地减少或预防继发性脑损伤。远程缺血性调节(RIC)是一种既定的治疗方式,已显示可通过影响炎症损伤改善不同临床环境下的患者预后。在一项临床试验中,RIC显示SB100和神经元特异性烯醇化酶得到改善。我们研究的目的是进一步阐明将RIC应用于创伤性脑损伤小鼠模型的机制和结果。
方法:我们对100只雄性C57BL小鼠进行了闭合颅骨皮质控制的撞击伤害。 TBI后两小时,将动物分为RIC组(n = 50)或假组(n = 50)。通过夹紧暴露的股动脉,我们通过六个4分钟的缺血和再灌注周期诱导RIC。在多个时间点测量了S100-B,神经元特异性烯醇化酶和神经胶质原纤维酸性蛋白的循环水平。每天还通过新颖的物体识别和旋转仪观察动物的认知和运动协调。在TBI后第5天对脑切片进行染色并评估其神经元损伤。
结果:在干预后24、48和72小时,RIC动物的识别指数明显高于假手术。在所有时间点,RIC动物的罗塔洛德潜伏期均高于假动物,在干预后120小时具有统计学意义。与假手术相比,RIC组显示出保留的认知功能和运动协调能力。关于苏木精和曙红以及脑切片的免疫组织化学染色,与假手术组相比,RIC组的神经元变性和星形胶质细胞减少的区域分别较少。 RIC动物和假动物之间的系统神经元标记没有显着差异。
结论:TBI小鼠模型在损伤后2小时可进行远程缺血调节,以保持认知功能和运动协调性。远端缺血性调理可以保留TBI后神经元和星形胶质细胞的活力,并具有作为临床无创且相对容易的方法来改善TBI后预后的潜力。
证据级别:治疗研究,随机对照试验,I级。

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