Department of Neurosurgery, Xijing Institute of Clinical Neuroscience, Xiing Hospital, Fourth Military Medical University, Xi'an 710032, Shaanxi Province, PR China.
Brain Res. 2010 Oct 1;1354:196-205. doi: 10.1016/j.brainres.2010.07.038. Epub 2010 Jul 21.
Traumatic brain injury (TBI) is a leading cause of mortality and disability among the young population. It has been shown that hydrogen gas (H(2)) exerts a therapeutic antioxidant activity by selectively reducing hydroxyl radical (OH, the most cytotoxic ROS). Recently, we have found that H(2) inhalation significantly improved the survival rate and organ damage of septic mice. In the present study, we investigated the effectiveness of H(2) therapy on brain edema, blood-brain barrier (BBB) breakdown, neurological dysfunction and injury volume in TBI-challenged rats. In addition, we investigated the effects of H(2) treatment on the changes of oxidative products and antioxidant enzymes in brain tissue of TBI-challenged rats. Hydrogen treatment was given by exposure to 2% H(2) from 5 min to 5h after sham or TBI operation, respectively. Here, we found that TBI-challenged rats showed significant brain injuries characterized by the increase of BBB permeability, brain edema and lesion volume as well as neurological dysfunction, which was significantly attenuated by 2% H(2) treatment. In addition, we found that the decrease of oxidative products and the increase of endogenous antioxidant enzymatic activities in the brain tissue may be associated with the protective effects of H(2) treatment in TBI-challenged rats. The present study supports that H(2) inhalation may be a more effective therapeutic strategy for patients with TBI.
创伤性脑损伤(TBI)是年轻人死亡和残疾的主要原因。研究表明,氢气(H₂)通过选择性还原羟基自由基(OH,最具细胞毒性的 ROS)发挥治疗性抗氧化活性。最近,我们发现 H₂吸入可显著提高脓毒症小鼠的存活率和器官损伤。在本研究中,我们研究了 H₂治疗对创伤性脑损伤大鼠脑水肿、血脑屏障(BBB)破坏、神经功能障碍和损伤体积的有效性。此外,我们还研究了 H₂治疗对创伤性脑损伤大鼠脑组织氧化产物和抗氧化酶变化的影响。H₂处理通过分别在假手术或 TBI 手术后 5 分钟至 5 小时暴露于 2%H₂来进行。在这里,我们发现 TBI 大鼠表现出明显的脑损伤特征,表现为 BBB 通透性增加、脑水肿和损伤体积增加以及神经功能障碍,2%H₂处理可显著减轻这些损伤。此外,我们发现脑组织中氧化产物的减少和内源性抗氧化酶活性的增加可能与 H₂处理对 TBI 大鼠的保护作用有关。本研究支持 H₂吸入可能是 TBI 患者更有效的治疗策略。