title: Hydrogen Sulfide Inhalation Improves  Neurological Outcome via NF-κB-Mediated  Inflammatory Pathway in a Rat Model of  Cardiac Arrest and Resuscitation.
abstract: OBJECTIVE
  The effects of H2S on cerebral inflammatory reaction after cardiac arrest (CA) and cardiopulmonary resuscitation (CPR) remain poorly understood. In this study, we investigated the effects of exogenous 40 ppm and 80 ppm H2S gas on inflammatory reaction and neurological outcome after CA/CPR.
  
  
  METHODS
  CA was induced by ventricular fibrillation and followed by CPR. Forty or 80 ppm H2S was inhaled for 1 h immediately following CPR. The levels of IL-1β, IL-6 and TNF-α, the myeloperoxidase (MPO) activity, the expression of iNOS and ICAM-1, and the phosphorylation and translocation of NF-κB were evaluated at 24 h after CA/ CPR. The tape removal test, survival rate and hippocampal neuronal counts were investigated at 14 d after CA/CPR.
  
  
  RESULTS
  CA/CPR induced significant increases in IL-1β, IL-6, TNF-α and MPO activity. The phosphorylation and translocation of NF-κB, and the expression of iNOS and ICAM-1 were increased significantly. Inhalation of 40 or 80 ppm H2S gas decreased these inflammatory cytokines. Furthermore, 40 or 80 ppm H2S inhibited the activation of NF-κB and the downstream proinflammatory mediators iNOS and ICAM-1. H2S inhalation also improved neurological function, 14-d survival rate, and reduced hippocampal neuronal loss.
  
  
  CONCLUSIONS
  These results indicated that inhalation of H2S protected against brain injury after CA/CPR. The mechanisms underlying protective effects of H2S were associated with the inhibition of CA/ CPR-induced inflammation reactions by reducing IL-1β, IL-6 and TNF-α, and concomitantly inhibiting the activation and infiltration of neutrophils. The beneficial effects of H2S might be mediated by downregulation of NF-κB and the downstream proinflammatory signaling pathway.
authors.forename: Xia
authors.initials: X
authors.lastname: Wei
authors.forename: Bing
authors.initials: B
authors.lastname: Zhang
authors.forename: Yu
authors.initials: Y
authors.lastname: Zhang
authors.forename: Hangbing
authors.initials: H
authors.lastname: Li
authors.forename: Long
authors.initials: L
authors.lastname: Cheng
authors.forename: Xiajie
authors.initials: X
authors.lastname: Zhao
authors.forename: Jinling
authors.initials: J
authors.lastname: Yin
authors.forename: Guonian
authors.initials: G
authors.lastname: Wang
mesh_terms: D000280:Administration, Inhalation; D000818:Animals; D001921:Brain / Q000187:drug effects / Q000276:immunology / Q000473:pathology; D001930:Brain Injuries / Q000209:etiology* / Q000276:immunology / Q000473:pathology / Q000517:prevention & control*; D016887:Cardiopulmonary Resuscitation; D002470:Cell Survival / Q000187:drug effects; D016207:Cytokines / Q000276:immunology; D064426:Gasotransmitters / Q000008:administration & dosage / Q000627:therapeutic use*; D006323:Heart Arrest / Q000150:complications*; D006862:Hydrogen Sulfide / Q000008:administration & dosage / Q000627:therapeutic use*; D008297:Male; D016328:NF-kappa B / Q000276:immunology*; D018696:Neuroprotective Agents / Q000008:administration & dosage / Q000627:therapeutic use*; D051381:Rats; D017207:Rats, Sprague-Dawley; D015398:Signal Transduction / Q000187:drug effects
chemical_list: D016207:Cytokines; D064426:Gasotransmitters; D016328:NF-kappa B; D018696:Neuroprotective Agents; D006862:Hydrogen Sulfide