title: Hydrogen-rich saline prevents early neurovascular dysfunction resulting from inhibition of oxidative stress in STZ-diabetic rats.
abstract: OBJECTIVE
  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.
  
  
  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.
authors.affiliation: Department of Ophthalmology, Shanghai Kongjiang Hospital, Shanghai, China.
authors.forename: Yanqing
authors.initials: Y
authors.lastname: Feng
authors.forename: Ruobing
authors.initials: R
authors.lastname: Wang
authors.forename: Jiajun
authors.initials: J
authors.lastname: Xu
authors.forename: Jingchuan
authors.initials: J
authors.lastname: Sun
authors.forename: Tao
authors.initials: T
authors.lastname: Xu
authors.forename: Qing
authors.initials: Q
authors.lastname: Gu
authors.forename: Xingwei
authors.initials: X
authors.lastname: Wu
mesh_terms: D000080242:8-Hydroxy-2'-Deoxyguanosine; D000447:Aldehydes / Q000378:metabolism; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D001813:Blood-Retinal Barrier / Q000187:drug effects; D015153:Blotting, Western; D001835:Body Weight; D019208:Brain-Derived Neurotrophic Factor / Q000378:metabolism; D003849:Deoxyguanosine / Q000031:analogs & derivatives / Q000378:metabolism; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism / Q000503:physiopathology / Q000517:prevention & control*; D003930:Diabetic Retinopathy / Q000378:metabolism / Q000503:physiopathology / Q000517:prevention & control*; D004596:Electroretinography; D004797:Enzyme-Linked Immunosorbent Assay; D008297:Male; D018384:Oxidative Stress / Q000187:drug effects*; D010088:Oxidoreductases / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D015861:Retinal Neovascularization / Q000503:physiopathology / Q000517:prevention & control*; D012965:Sodium Chloride / Q000494:pharmacology*; D016708:Synaptophysin / Q000378:metabolism
chemical_list: D000447:Aldehydes; D001786:Blood Glucose; D019208:Brain-Derived Neurotrophic Factor; D016708:Synaptophysin; D012965:Sodium Chloride; D000080242:8-Hydroxy-2'-Deoxyguanosine; D010088:Oxidoreductases; D003849:Deoxyguanosine; C027576:4-hydroxy-2-nonenal