来自吉林大学第一附属医院神经外科的研究，文章发表在Neurol Res上。

动物模型：两动脉结扎一过性脑缺血模型。120只动物，分成sham,sham+H2,缺血和缺血+H2，每组30只。2%氢气呼吸，在手术后即刻到3小时。认知功能采用水迷宫评价。海马Ca1神经细胞损伤采用HE染色（应该用尼染或Tunel更好一些）并进行计数。氧化损伤检测MDA、8-iso-prostaglandin F2alpha、SOD和CAT。结果发现行为学证明动物记忆力提高，神经细胞计数从3升高到21。Moreover, hydrogen gas made higher levels of MDA and 8-iso-PGF2α in the ischemic rats attenuate to 3.2±0.2, 3.5±0.5, 3.4±0.3 and 26.4±2.3, 28.2±2.6, 26.8±2.1 at reperfusion 4, 24, and 72 hours, respectively (P<0.01 versus ischemia group at each indicated time)这个内容似乎有误，少了一组数据。By contrast, the activities of superoxide dismutase and catalase damaged by ischemia/reperfusion recovered to 129.7±14.8, 100.5±12.2 and 11.4±0.8, 9.6±1.1 at reperfusion 24 and 72 hours, respectively (P<0.01 versus ischemia group at each indicated time)这个也少了一组数据。结果表明，氢气呼吸可以减少氧化应激保护脑缺血后神经功能损伤。

Neurol Res. 2012 Feb 2. [Epub ahead of print]

Inhalation of hydrogen gas attenuates cognitive impairment in transient cerebral ischemia via inhibition of oxidative stress.

Ge P, Zhao J, Li S, Ding Y, Yang F, Luo Y.

Affiliations: 1: Department of Neurosurgery, 1st Bethune Hospital of Jilin University, Changchun, China 3: Department of Neurosurgery, Wayne State University School of Medicine, Detroit, MI, USA

Publication date: 2012-01-01

Objective: To investigate the effects of inhalation of hydrogen gas on cognitive impairment induced by transient cerebral ischemia and its potential mechanism. Methods: Two-vessel occlusion rat model was used to produce 10-minute transient global cerebral ischemia. One hundred and twenty male Wistar rats were randomly divided into sham, sham+H2, ischemia, and ischemia+H2 groups (n=30 each group). Inhalation of 2% hydrogen gas was performed immediately at the end of operation and lasted for 3 hours. Cognitive function of rats was evaluated via Morris water maze. Neuronal damage in the CA1 region was quantified according to their morphological changes revealed by hematoxylin-eosin staining. The levels of oxidative stress products malondialdehyde (MDA) and 8-iso-prostaglandin F2alpha, and the activities of anti-oxidative enzymes catalase and superoxide dismutase were measured to investigate the effects of inhalation of hydrogen gas on oxidative stress. Results: Inhalation of hydrogen gas decreased significantly the average latency of the ischemic rats in finding hidden platform and elongated markedly their retention in the target quadrant. The neuronal density 3.3±2.1 cells/mm in CA1 region of the ischemic rats increased to 21.7±2.6 cells/mm after they were treated with hydrogen gas. Moreover, hydrogen gas made higher levels of MDA and 8-iso-PGF2α in the ischemic rats attenuate to 3.2±0.2, 3.5±0.5, 3.4±0.3 and 26.4±2.3, 28.2±2.6, 26.8±2.1 at reperfusion 4, 24, and 72 hours, respectively (P<0.01 versus ischemia group at each indicated time). By contrast, the activities of superoxide dismutase and catalase damaged by ischemia/reperfusion recovered to 129.7±14.8, 100.5±12.2 and 11.4±0.8, 9.6±1.1 at reperfusion 24 and 72 hours, respectively (P<0.01 versus ischemia group at each indicated time). Conclusion: Inhalation of hydrogen gas could attenuate cognitive impairment in the ischemic rats. This protection is associated with decreased neuronal death in CA1 region and inhibition of oxidative stress.

Keywords: Transient global cerebral ischemia; Cognitive impairment; Hydrogen gas; Oxidative stress; Neuronal death

DOI: http://dx.doi.org/10.1179/1743132812Y.0000000002