糖尿病可通过氧化应激和硝化应激的共同作用导致神经毒性和血管通透性改变，导致糖尿病视网膜病变。过去的研究发现，富氢生理盐水不仅具有相当的抗氧化和抗炎性质，但也抑制氧化应激诱导的损伤。在本研究中，我们评估了富氢生理盐水神经血管功能障碍和氧化应激的动物模型(大鼠)糖尿病视网膜病变的影响。

　　材料与方法：雄性Sprague-Dawley大鼠用链脲佐菌素(STZ)诱导的糖尿病(DM)模型。腹腔内注射5毫升/公斤氢饱和或纯盐水每天一次，连续一个月。视网膜电图(ERG)评价视觉功能，牛血清白蛋白(BSA)的荧光评价血视网膜屏障(BRB)的完整性。光镜观察视网膜内层的组织学改变。氧化应激的生物标志物包括4 - 羟基(4-HNE)和8 - 羟基-2 - 脱氧鸟苷(8-OH-dG的)，及超氧化物歧化酶，谷胱甘肽过氧化物酶，谷胱甘肽还原酶和谷胱甘肽转移酶等抗氧化酶，酶联免疫吸附法(ELISA)和免疫印迹法检测突触素和脑源性神经营养因子(BDNF)水平。结果发现：STZ糖尿病大鼠明显减少b波的振幅和振荡电位，DM-BRB故障和内层视网膜的组织学改变，所有这一切都可被富氢生理盐水治疗后抑制。此外，富氢生理盐水可减少氧化应激，提高抗氧化酶活性和保存在糖尿病大鼠视网膜突触素和脑源性神经营养因子的水平。结论：基于其抑制氧化应激和抗氧化酶的上调，我们认为，富氢生理盐水是一个潜在的有价值的治疗方法，治疗糖尿病视网膜病变。

　　Curr Eye Res.2012 Dec 19. [Epub ahead of print]

　　Hydrogen-Rich Saline Prevents Early Neurovascular Dysfunction Resulting from Inhibition of Oxidative Stress in STZ-Diabetic Rats.

　　Feng Y, Wang R, Xu J, Sun J, Xu T, Gu Q, Wu X.

　　Source

　　Department of Ophthalmology, Shanghai Kongjiang Hospital, Shanghai , China.

　　Abstract

　　ABSTRACT Purpose: Diabetic retinopathy (DR) is characterized by increased oxidative and nitrosative stress, both of which lead to neurotoxicity and vascular permeability. Previous studies on a variety of organs indicate that hydrogen-rich saline not only has considerable antioxidant and anti-inflammatory properties, but also suppresses oxidative stress-induced injury. In the present study, we assessed the effects of hydrogen-rich saline on neurovascular dysfunction and oxidative stress in an animal model (rat) of DR. Materials and Methods: Male Sprague-Dawley rats with streptozotocin (STZ)-induced diabetes mellitus (DM) were injected intraperitoneally with 5?ml/kg hydrogen-saturated (experimental) or plain(control) saline daily for one month. Visual function and blood-retinal barrier(BRB) integrity were evaluated by electroretinography (ERG) and bovine serum albumin (BSA)-fluorescence, respectively. Histological changes in the inner retina were assessed by light microscopy. Biomarkers of oxidative stress, including 4-hydroxynonenal (4-HNE) and 8-hydroxy-2-deoxyguanosine (8-OH-dG), and antioxidant enzymes, including superoxide dismutase, glutathione peroxidase, glutathione reductase and glutathione transferase, were evaluated by ELISA. Synaptophysin and brain-derived neurotrophic factor (BDNF) levels were measured by immunoblotting. Results: STZ-diabetic rats were marked by clearly reduced b-wave amplitudes and oscillatory potentials, DM-related BRB breakdown and histological changes in the inner retina, all of which were suppressed following treatment with hydrogen-rich saline. Furthermore, hydrogen-rich saline reduced oxidative stress, increased antioxidant enzyme activities and preserved synaptophysin and BDNF levels in the diabetic rat retina. Conclusions: Based on its inhibition of oxidative stress and up-regulation of anti-oxidative enzymes, we conclude that hydrogen-rich saline is a potentially valuable therapeutic modality for the treatment of DR.