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The Changes of Brain Edema and Neurological Outcome, and the Probable Mechanisms in Diffuse Traumatic Brain Injury Induced in Rats with the History of Exercise
Cellular and Molecular Neurobiology ( IF 4 ) Pub Date : 2019-12-14 , DOI: 10.1007/s10571-019-00753-w
Nasrin Soltani 1 , Zahra Soltani 2 , Mohammad Khaksari 3 , Ghasem Ebrahimi 4 , Mojdeh Hajmohammmadi 1 , Maryam Iranpour 5
Affiliation  

Abstract

Since no definitive treatment has been suggested for diffuse traumatic brain injury (TBI), and also as the effect of exercise has been proven to be beneficial in neurodegenerative diseases, the effect of endurance exercise on the complications of TBI along with its possible neuroprotective mechanism was investigated in this study. Our objective was to find out whether previous endurance exercise influences brain edema and neurological outcome in TBI. We also assessed the probable mechanism of endurance exercise effect in TBI. Rats were randomly assigned into four groups of sham, TBI, exercise + sham and exercise + TBI. Endurance exercise was carried out before TBI. Brain edema was assessed by calculating the percentage of brain water content 24 h after the surgery. Neurological outcome was evaluated by obtaining veterinary coma scale (VCS) at − 1, 1, 4 and 24 h after the surgery. Interleukin-1β (IL-1β), total antioxidant capacity (TAC), malondialdehyde (MDA), protein carbonyl and histopathological changes were evaluated 24 h after the surgery. Previous exercise prevented the increase in brain water content, MDA level, histopathological edema and apoptosis following TBI. The reduction in VCS in exercise + TBI group was lower than that of TBI group. In addition, a decrease in the level of serum IL-1β and the content of brain protein carbonyl was reported in exercise + TBI group in comparison with the TBI group. We suggest that the previous endurance exercise prevents brain edema and improves neurological outcome following diffuse TBI, probably by reducing apoptosis, inflammation and oxidative stress.



中文翻译:

运动史大鼠脑水肿和神经系统疾病的变化以及弥漫性颅脑损伤的可能机制

摘要

由于尚未建议对弥漫性颅脑损伤(TBI)进行彻底治疗,而且运动已被证明对神经退行性疾病有益,因此耐力运动对TBI并发症的影响及其可能的神经保护机制为:在这项研究中进行了调查。我们的目的是发现以前的耐力运动是否会影响TBI的脑水肿和神经系统结果。我们还评估了TBI中耐力运动效果的可能机制。将大鼠随机分为假手术,TBI,运动+假手术和运动+ TBI四组。在进行TBI之前进行了耐力运动。通过计算手术后24小时的脑水含量百分比来评估脑水肿。通过获得− 1的兽医昏迷量表(VCS)评估神经系统结局 手术后1、4和24小时。术后24小时评估白细胞介素-1β(IL-1β),总抗氧化能力(TAC),丙二醛(MDA),羰基蛋白和组织病理学变化。先前的运动可防止TBI后脑含水量,MDA水平,组织病理学水肿和细胞凋亡的增加。运动+ TBI组的VCS降低低于TBI组。另外,与TBI组相比,运动+ TBI组血清IL-1β水平和脑蛋白羰基含量降低。我们建议,以前的耐力运动可预防脑水肿并改善弥漫性TBI后的神经功能,可能是通过减少细胞凋亡,炎症和氧化应激。术后24小时评估丙二醛(MDA),羰基蛋白和组织病理学变化。先前的运动可防止TBI后脑含水量,MDA水平,组织病理学水肿和细胞凋亡的增加。运动+ TBI组的VCS降低低于TBI组。另外,与TBI组相比,运动+ TBI组血清IL-1β水平和脑蛋白羰基含量降低。我们建议,以前的耐力运动可预防脑水肿并改善弥漫性TBI后的神经功能,可能是通过减少细胞凋亡,炎症和氧化应激。术后24小时评估丙二醛(MDA),羰基蛋白和组织病理学变化。先前的运动可防止TBI后脑含水量,MDA水平,组织病理学水肿和细胞凋亡的增加。运动+ TBI组的VCS降低低于TBI组。另外,与TBI组相比,运动+ TBI组血清IL-1β水平和脑蛋白羰基含量降低。我们建议,以前的耐力运动可预防脑水肿并改善弥漫性TBI后的神经功能,可能是通过减少细胞凋亡,炎症和氧化应激。TBI后的组织病理学水肿和细胞凋亡。运动+ TBI组的VCS降低低于TBI组。另外,与TBI组相比,运动+ TBI组血清IL-1β水平和脑蛋白羰基含量降低。我们建议,以前的耐力运动可预防脑水肿并改善弥漫性TBI后的神经功能,可能是通过减少细胞凋亡,炎症和氧化应激。TBI后的组织病理学水肿和细胞凋亡。运动+ TBI组的VCS降低低于TBI组。另外,与TBI组相比,运动+ TBI组血清IL-1β水平和脑蛋白羰基含量降低。我们建议,以前的耐力运动可预防脑水肿并改善弥漫性TBI后的神经功能,可能是通过减少细胞凋亡,炎症和氧化应激。

更新日期:2020-04-20
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