Kızılay Zahir, Erken Haydar Ali, Çetin Nesibe Kahraman, Aktaş Serdar, Abas Burçin İrem, Yılmaz Ali
Department of Neurosurgery, Faculty of Medicine, Adnan Menderes University, Aydin, Turkey.
Department of Physiology, Faculty of Medicine, Balikesir University, Balikesir, Turkey.
Neural Regen Res. 2016 Oct;11(10):1660-1665. doi: 10.4103/1673-5374.193247.
The aim of this study was to investigate the effects of boric acid in experimental acute sciatic nerve injury. Twenty-eight adult male rats were randomly divided into four equal groups ( = 7): control (C), boric acid (BA), sciatic nerve injury (I), and sciatic nerve injury + boric acid treatment (BAI). Sciatic nerve injury was generated using a Yasargil aneurysm clip in the groups I and BAI. Boric acid was given four times at 100 mg/kg to rats in the groups BA and BAI after injury (by gavage at 0, 24, 48 and 72 hours) but no injury was made in the group BA. electrophysiological tests were performed at the end of the day 4 and sciatic nerve tissue samples were taken for histopathological examination. The amplitude of compound action potential, the nerve conduction velocity and the number of axons were significantly lower and the myelin structure was found to be broken in group I compared with those in groups C and BA. However, the amplitude of the compound action potential, the nerve conduction velocity and the number of axons were significantly greater in group BAI than in group I. Moreover, myelin injury was significantly milder and the intensity of nuclear factor kappa B immunostaining was significantly weaker in group BAI than in group I. The results of this study show that administration of boric acid at 100 mg/kg after sciatic nerve injury in rats markedly reduces myelin and axonal injury and improves the electrophysiological function of injured sciatic nerve possibly through alleviating oxidative stress reactions.
本研究的目的是探讨硼酸对实验性急性坐骨神经损伤的影响。将28只成年雄性大鼠随机分为四组，每组7只：对照组（C）、硼酸组（BA）、坐骨神经损伤组（I）和坐骨神经损伤+硼酸治疗组（BAI）。在I组和BAI组中，使用Yasargil动脉瘤夹造成坐骨神经损伤。损伤后，对BA组和BAI组的大鼠以100mg/kg的剂量给予硼酸4次（在0、24、48和72小时通过灌胃给药），而BA组不造成损伤。在第4天结束时进行电生理测试，并取坐骨神经组织样本进行组织病理学检查。与C组和BA组相比，I组的复合动作电位幅度、神经传导速度和轴突数量显著降低，且发现髓鞘结构破坏。然而，BAI组的复合动作电位幅度、神经传导速度和轴突数量显著高于I组。此外，BAI组的髓鞘损伤明显较轻，核因子κB免疫染色强度明显弱于I组。本研究结果表明，大鼠坐骨神经损伤后给予100mg/kg的硼酸可能通过减轻氧化应激反应，显著减轻髓鞘和轴突损伤，并改善受损坐骨神经的电生理功能。
