title: Sodium Sulfide, a Hydrogen Sulfide-Releasing Molecule, Attenuates Acute Cerebral Ischemia in Rats.
abstract: Acute cerebral ischemia may lead to ischemic stroke, which is a major cause of death and disability worldwide. Hydrogen sulfide (H2 S) functions importantly in mammalian systems. The present work was designed to study the effect of sodium sulfide, a donor of H2 S, on acute cerebral ischemia.
  
  
  
  Acute cerebral focal ischemia was produced by middle cerebral artery occlusion (MCAO) in Sprague-Dawley (SD) rats. Bilateral vertebral arteries and common carotid arteries were blocked to establish cerebral global ischemia in SD rats. Acute cerebral anoxia was produced by hypobaric anoxia in C57BL/6 mice and hypoxic anoxia in SD rats. Nimodipine and aspirin were set as positive control separately.
  
  
  
  Infarct size after MCAO was decreased by sodium sulfide. Sodium sulfide improved cerebral energy metabolism after cerebral global ischemia and prolonged survival time of animals with acute cerebral anoxia. In addition, increased cerebral blood flow and decreased cerebrovascular resistance, blood viscosity, and thrombogenesis were observed in animals treated with sodium sulfide. In cultured neurons, sodium sulfide increased cell viability and decreased cell apoptosis induced by oxygen-glucose deprivation.
  
  
  
  Sodium sulfide, a H2 S donor, presents protective effect on acute cerebral ischemia, and might be a promising therapeutic drug.
authors.affiliation: Department of Pharmacy, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
authors.forename: Hao-Qiang
authors.initials: HQ
authors.lastname: Shi
authors.affiliation: Department of Pharmacology, Second Military Medical University, Shanghai, China.
authors.forename: Ying
authors.initials: Y
authors.lastname: Zhang
authors.affiliation: Department of Pharmacology, Second Military Medical University, Shanghai, China.
authors.forename: Ming-He
authors.initials: MH
authors.lastname: Cheng
authors.affiliation: Department of Pharmacology, Second Military Medical University, Shanghai, China.
authors.forename: Bo-Shi
authors.initials: BS
authors.lastname: Fan
authors.affiliation: Department of Pharmacology, Second Military Medical University, Shanghai, China.
authors.forename: Jia-Sheng
authors.initials: JS
authors.lastname: Tian
authors.affiliation: Department of Pharmacology, Second Military Medical University, Shanghai, China.
authors.forename: Jian-Guang
authors.initials: JG
authors.lastname: Yu
authors.affiliation: Department of Pharmacy, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
authors.forename: Bing
authors.initials: B
authors.lastname: Chen
mesh_terms: D000208:Acute Disease; D000704:Analysis of Variance; D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D001241:Aspirin / Q000627:therapeutic use; D001794:Blood Pressure / Q000187:drug effects; D002470:Cell Survival / Q000187:drug effects; D002478:Cells, Cultured; D002560:Cerebrovascular Circulation / Q000187:drug effects; D004195:Disease Models, Animal; D004285:Dogs; D004305:Dose-Response Relationship, Drug; D004569:Electroencephalography; D005343:Fibrinolytic Agents / Q000627:therapeutic use; D006339:Heart Rate / Q000187:drug effects; D020244:Infarction, Middle Cerebral Artery / Q000150:complications / Q000188:drug therapy*; D051379:Mice; D008810:Mice, Inbred C57BL; D009422:Nervous System Diseases / Q000188:drug therapy / Q000209:etiology; D018696:Neuroprotective Agents / Q000627:therapeutic use*; D009553:Nimodipine / Q000627:therapeutic use; D051381:Rats; D017207:Rats, Sprague-Dawley; D013440:Sulfides / Q000627:therapeutic use*; D013997:Time Factors
chemical_list: D005343:Fibrinolytic Agents; D018696:Neuroprotective Agents; D013440:Sulfides; D009553:Nimodipine; D001241:Aspirin; C033479:sodium sulfide
keywords: Acute cerebral ischemia; Hydrogen sulfide; Sodium sulfide; Stroke