title: Hydrogen-rich saline attenuates vascular smooth muscle cell proliferation             and neointimal hyperplasia by inhibiting reactive oxygen species production and             inactivating the Ras-ERK1/2-MEK1/2 and Akt pathways.
abstract: Hydrogen-rich saline has been reported to prevent neointimal hyperplasia             induced by carotid balloon injury. The purpose of the present study was to further             investigate the molecular mechanisms underlying this phenomenon. Daily injection             of a hydrogen-rich saline solution (HRSS) in rats was employed to study the effect             of hydrogen on balloon injury-induced neointimal hyperplasia and the neointima/media             ratio was assessed. HRSS significantly decreased the neointima area and neointima/media             ratio in a dose-dependent manner. In vitro effects of hydrogen on fetal bovine             serum (FBS)-induced vascular smooth muscle cell (VSMC) proliferation were also             investigated. Hydrogen-rich medium (HRM) inhibited rat VSMC proliferation and             migration induced by 10% FBS. FBS-induced reactive oxygen species (ROS) production             and activation of intracellular Ras, MEK1/2, ERK1/2, proliferative cell nuclear             antigen (PCNA), Akt were significantly inhibited by HRM. In addition, HRM blocked             FBS-induced progression from the G0/G1 to the S-phase and increased the apoptosis             rate of VSMCs. These results showed that hydrogen-rich saline was able to attenuate             FBS-induced VSMC proliferation and neointimal hyperplasia by inhibiting ROS production             and inactivating the Ras-ERK1/2-MEK1/2 and Akt pathways. Thus, HRSS may have potential             therapeutic relevance for the prevention of human restenosis.
authors: Department of Cardiology, The Third Hospital of Hebei Medical University, Shijiazhuang, Hebei 050051, PR China.
authors: Yali
authors: Y
authors: Chen
authors: Jinyao
authors: J
authors: Jiang
authors: Huibing
authors: H
authors: Miao
authors: Xingjuan
authors: X
authors: Chen
authors: Xuejun
authors: X
authors: Sun
authors: Yongjun
authors: Y
authors: Li
mesh_terms: D015906:Angioplasty, Balloon, Coronary / Q000009:adverse effects; D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D059447:Cell Cycle Checkpoints / Q000187:drug effects; D002465:Cell Movement / Q000187:drug effects; D049109:Cell Proliferation / Q000187:drug effects; D002478:Cells, Cultured; D023903:Coronary Restenosis / Q000517:prevention & control; D048049:Extracellular Signal-Regulated MAP Kinases / Q000037:antagonists & inhibitors; D006859:Hydrogen / Q000494:pharmacology*; D006965:Hyperplasia / Q000188:drug therapy*; D020935:MAP Kinase Signaling System / Q000187:drug effects*; D008297:Male; D020928:Mitogen-Activated Protein Kinases / Q000037:antagonists & inhibitors; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000378:metabolism*; D058426:Neointima / Q000473:pathology; D051057:Proto-Oncogene Proteins c-akt / Q000037:antagonists & inhibitors / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D017382:Reactive Oxygen Species / Q000378:metabolism; D012965:Sodium Chloride / Q000494:pharmacology*; D014945:Wound Healing; D020663:ras Guanine Nucleotide Exchange Factors / Q000037:antagonists & inhibitors
chemical_list: D017382:Reactive Oxygen Species; D020663:ras Guanine Nucleotide Exchange Factors; D012965:Sodium Chloride; D006859:Hydrogen; D051057:Proto-Oncogene Proteins c-akt; D048049:Extracellular Signal-Regulated MAP Kinases; D020928:Mitogen-Activated Protein Kinases