Military Medicine Research Unit, Test and Evaluation Command, Japan Ground Self-Defense Force, Setagaya, Tokyo, Japan.
Division of Hematology, Department of Internal Medicine, National Defense Medical College, Tokorozawa, Saitama, Japan.
PLoS One. 2020 Apr 2;15(4):e0230774. doi: 10.1371/journal.pone.0230774. eCollection 2020.
Oxidative stress is considered to be involved in the pathogenesis of primary blast-related traumatic brain injury (bTBI). We evaluated the effects of ascorbic acid 2-glucoside (AA2G), a well-known antioxidant, to control oxidative stress in rat brain exposed to laser-induced shock waves (LISWs). The design consisted of a controlled animal study using male 10-week-old Sprague-Dawley rats. The study was conducted at the University research laboratory. Low-impulse (54 Pa•s) LISWs were transcranially applied to rat brain. Rats were randomized to control group (anesthesia and head shaving, n = 10), LISW group (anesthesia, head shaving and LISW application, n = 10) or LISW + post AA2G group (AA2G administration after LISW application, n = 10) in the first study. In another study, rats were randomized to control group (n = 10), LISW group (n = 10) or LISW + pre and post AA2G group (AA2G administration before and after LISW application, n = 10). The measured outcomes were as follows: (i) motor function assessed by accelerating rotarod test; (ii) levels of 8-hydroxy-2'-deoxyguanosine (8-OHdG), an oxidative stress marker; (iii) ascorbic acid in each group of rats. Ascorbic acid levels were significantly decreased and 8-OHdG levels were significantly increased in the cerebellum of the LISW group. Motor coordination disorder was also observed in the group. Prophylactic AA2G administration significantly increased the ascorbic acid levels, reduced oxidative stress and mitigated the motor dysfunction. In contrast, the effects of therapeutic AA2G administration alone were limited. The results suggest that the prophylactic administration of ascorbic acid can reduce shock wave-related oxidative stress and prevented motor dysfunction in rats.
氧化应激被认为与原发性爆炸相关的创伤性脑损伤（bTBI）的发病机制有关。我们评估了抗坏血酸 2-葡糖苷（AA2G）的作用，AA2G 是一种众所周知的抗氧化剂，可控制暴露于激光诱导冲击波（LISW）的大鼠大脑中的氧化应激。该设计包括一项使用 10 周龄雄性 Sprague-Dawley 大鼠的对照动物研究。该研究在大学研究实验室进行。低脉冲（54 Pa•s）LISW 经颅应用于大鼠大脑。大鼠随机分为对照组（麻醉和剃光头，n = 10）、LISW 组（麻醉、剃光头和 LISW 应用，n = 10）或 LISW+AA2G 后组（LISW 应用后给予 AA2G，n = 10）。在另一项研究中，大鼠随机分为对照组（n = 10）、LISW 组（n = 10）或 LISW+AA2G 预和后组（LISW 应用前和后给予 AA2G，n = 10）。测量的结果如下：（i）加速旋转棒试验评估的运动功能；（ii）氧化应激标志物 8-羟基-2'-脱氧鸟苷（8-OHdG）的水平；（iii）各组大鼠中的抗坏血酸。LISW 组小脑的抗坏血酸水平显著降低，8-OHdG 水平显著升高。该组还观察到运动协调障碍。预防性 AA2G 给药可显著增加抗坏血酸水平，减轻氧化应激并减轻运动功能障碍。相比之下，单独给予治疗性 AA2G 给药的效果有限。结果表明，预防性给予抗坏血酸可以减轻与冲击波相关的氧化应激，并防止大鼠的运动功能障碍。
